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        <title>Vascular Pharmacology via MedWorm.com</title>
        <description>MedWorm.com provides a medical RSS filtering service. Over 6000 RSS medical sources are combined and output via different filters. This feed contains the latest items from the 'Vascular Pharmacology' source.</description>
        <link><![CDATA[http://www.medworm.com/rss/search.php?qu=Vascular+Pharmacology&t=Vascular+Pharmacology&s=Search&f=source]]></link>
        <lastBuildDate>Wed, 08 Feb 2012 14:04:34 +0100</lastBuildDate>
        <item>
            <title>Arginase inhibition alleviates hypertension associated with diabetes: Effect on endothelial dependent relaxation and NO production.</title>
            <link>http://www.medworm.com/index.php?rid=5643134&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22281732%26dopt%3DAbstract</link>
            <description>In conclusion, arginase inhibition alleviates hypertension in diabetes through a mechanism involving prevention of the impairment in endothelial dependent relaxation and NO production.
    PMID: 22281732 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5643134</comments>
            <pubDate>Tue, 17 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Vascular effects of glycoprotein130 ligands - Part II: Biomarkers and therapeutic targets.</title>
            <link>http://www.medworm.com/index.php?rid=5625643&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22245786%26dopt%3DAbstract</link>
            <description>Authors: Demyanets S, Huber K, Wojta J
    Abstract
    Glycoprotein130 (gp130) ligands are defined by the use of the common receptor subunit gp130 and comprise interleukin (IL)-6, oncostatin M (OSM), IL-11, leukemia inhibitory factor (LIF), cardiotrophin-1 (CT-1), cardiotrophin-like cytokine (CLC), ciliary neurotrophic factor (CNTF), IL-27 and neuropoietin (NP). In part I of this review we addressed the pathophysiological functions of gp130 ligands with respect to the vascular wall. In part II of this review on the vascular effects of gp130 ligands we will discuss data about possible use of these molecules as biomarkers to predict development or progression of cardiovascular diseases. Furthermore, the possibility to modulate circulating levels of gp130 ligands or their tissue expression b...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625643</comments>
            <pubDate>Sun, 08 Jan 2012 05:00:00 +0100</pubDate>
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        <item>
            <title>Panax notoginseng and its components decreased hypertension via stimulation of endothelial-dependent vessel dilatation.</title>
            <link>http://www.medworm.com/index.php?rid=5625644&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22239978%26dopt%3DAbstract</link>
            <description>CONCLUSION: Ginsenoside Rb1 and Rg1 increased endothelial-dependent vessel dilatation through the activation of NO by modulating the PI3K/Akt/eNOS pathway and l-arginine transport in endothelial cells. These findings may have important implications for understanding the mechanisms of clinical efficacy of the herb P.N. when used in the regulation of blood pressure.
    PMID: 22239978 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5625644</comments>
            <pubDate>Tue, 03 Jan 2012 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5625644</guid>        </item>
        <item>
            <title>The BK(Ca) channels deficiency as a possible reason for radiation-induced vascular hypercontractility.</title>
            <link>http://www.medworm.com/index.php?rid=5579864&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22226998%26dopt%3DAbstract</link>
            <description>Authors: Kyrychenko S, Tishkin S, Dosenko V, Ivanova I, Novokhatska T, Soloviev A
    Abstract
    It is likely that large-conductance Ca(2+)-activated K(+) (BK(Ca)) channels channelopathy tightly involved in vascular malfunctions and arterial hypertension development. In the present study, we compared the results of siRNAs-induced α-BK(Ca) gene silencing and vascular abnormalities produced by whole-body ionized irradiation in rats. The experimental design comprised RT-PCR and patch clamp technique, thoracic aorta smooth muscle (SM) contractile recordings and arterial blood pressure (BP) measurements on the 30th day after whole body irradiation (6Gy) and following siRNAs KCNMA1 gene silencing in vivo. The expression profile of BK(Ca) mRNA transcripts in SM was significantly decreased in s...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5579864</comments>
            <pubDate>Thu, 29 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5579864</guid>        </item>
        <item>
            <title>Endothelial nitric oxide and 15-lipoxygenase-1 metabolites independently mediate relaxation of the rabbit aorta.</title>
            <link>http://www.medworm.com/index.php?rid=5551875&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22197897%26dopt%3DAbstract</link>
            <description>Authors: Aggarwal NT, Gauthier KM, Campbell WB
    Abstract
    Endothelial 15-lipoxygenase-1 (15-LO-1) metabolites of arachidonic acid (AA), 11,12,15-trihydroxyeicosatrienoic acid (THETA) and 15-hydroxy-11,12-epoxyeicosatrienoic acid (HEETA) and nitric oxide (NO) mediate relaxations to acetylcholine (ACH). However, interactions between NO and the 15-LO-1 pathway have not been explored. Therefore, the effect of physiological and pharmacological concentrations of NO on 15-LO activity and relaxation was studied in rabbit aorta. In indomethacin-treated aortic rings, maximal ACH relaxations of 91.3±4.0%, decreased to 54.5±3.0% by the NO synthase inhibitor, nitro-l-arginine (LNA), to 49.8±3% by the guanylate cyclase (GC) inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one, to 63.7±4.9% b...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5551875</comments>
            <pubDate>Fri, 16 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5551875</guid>        </item>
        <item>
            <title>Vascular effects of glycoprotein130 ligands - Part I: Pathophysiological role.</title>
            <link>http://www.medworm.com/index.php?rid=5551874&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22197898%26dopt%3DAbstract</link>
            <description>Authors: Demyanets S, Huber K, Wojta J
    Abstract
    The vessel wall is no longer considered as only an anatomical barrier for blood cells but is recognized as an active endocrine organ. Dysfunction of the vessel wall occurs in various disease processes including atherosclerosis, hypertension, peripheral artery disease, aneurysms, and transplant and diabetic vasculopathies. Different cytokines were shown to modulate the behavior of the cells, which constitute the vessel wall such as immune cells, endothelial cells and smooth muscle cells. Glycoprotein 130 (gp130) is a common cytokine receptor that controls the activity of a group of cytokines, namely, interleukin (IL)-6, oncostatin M (OSM), IL-11, ciliary neurotrophic factor (CNTF), leukemia inhibitory factor (LIF), cardiotrophin-1 (CT-...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5551874</comments>
            <pubDate>Fri, 16 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5551874</guid>        </item>
        <item>
            <title>Biomarkers of inflammation and endothelial function: The holy grail of experimental and clinical medicine?</title>
            <link>http://www.medworm.com/index.php?rid=5551873&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22198643%26dopt%3DAbstract</link>
            <description>Authors: Biasucci LM, Cardillo MT
    Abstract
    Drug induced vasculitides in humans are relatively rare diseases, resembling drug-induced vasculitis in rodents and primary idiopathic vasculitis. Because of their exquisite inflammatory nature, vascular lesions in these conditions release a large amount of bioactive molecules and activate multiple cell types, including endothelial cells, neutrophils, monocytes and T-lymphocytes, all of which might be in principle used as biomarkers of the underlying disease. Although each vasculitis may have specific features, the potential biomarkers released remain largely non-specific, raising the question of whether they represent a useful clinical tool. Low specificity, short half-lives and analytical weaknesses are all issues that must be resolved b...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5551873</comments>
            <pubDate>Fri, 16 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5551873</guid>        </item>
        <item>
            <title>Mechanisms underlining gender differences in Phenylephrine contraction of normoglycaemic and short-term Streptozotocin-induced diabetic WKY rat aorta.</title>
            <link>http://www.medworm.com/index.php?rid=5537272&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22172524%26dopt%3DAbstract</link>
            <description>In conclusion, there is an endothelium-dependent gender difference in the effect of short term diabetes on vascular tissue reactivity which is COX mediated.
    PMID: 22172524 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537272</comments>
            <pubDate>Tue, 06 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537272</guid>        </item>
        <item>
            <title>Sulforaphane suppresses vascular adhesion molecule-1 expression in TNF-α-stimulated mouse vascular smooth muscle cells: Involvement of the MAPK, NF-κB and AP-1 signaling pathways.</title>
            <link>http://www.medworm.com/index.php?rid=5537276&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22155163%26dopt%3DAbstract</link>
            <description>This study suggests that sulforaphane inhibits the adhesive capacity of VSMC and downregulates the TNF-α-mediated induction of VCAM-1 in VSMC by inhibiting the MAPK, NF-κB and AP-1 signaling pathways and intracellular ROS production. Thus, sulforaphane may have beneficial effects to suppress inflammation within the atherosclerotic lesion.
    PMID: 22155163 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537276</comments>
            <pubDate>Sun, 04 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537276</guid>        </item>
        <item>
            <title>Salvianolic acid B inhibits SDF-1α-stimulated cell proliferation and migration of vascular smooth muscle cells by suppressing CXCR4 receptor.</title>
            <link>http://www.medworm.com/index.php?rid=5537274&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22166584%26dopt%3DAbstract</link>
            <description>In conclusion, suppressing the expression levels of CXCR4 receptor and downstream molecules of SDF-1α/CXCR4 axis could possibly explain one of the pharmacological mechanisms of Sal B on prevention of cell proliferation, migration and subsequently neointimal hyperplasia.
    PMID: 22166584 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537274</comments>
            <pubDate>Sun, 04 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537274</guid>        </item>
        <item>
            <title>Activation of hexosamine pathway impairs nitric oxide (NO)-dependent arteriolar dilations by increased protein O-GlcNAcylation.</title>
            <link>http://www.medworm.com/index.php?rid=5537278&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22155161%26dopt%3DAbstract</link>
            <description>Authors: Beleznai T, Bagi Z
    Abstract
    We hypothesized that under high glucose conditions, activation of the hexosamine pathway leads to impaired nitric oxide (NO)-dependent arteriolar dilation. Skeletal muscle arterioles (diameter: ~160μm) isolated from male Wistar rats were exposed to normal glucose (NG, 5.5mmol/L) or high glucose concentrations (HG, 30mmol/L, for 2h) and agonist-induced diameter changes were measured with videomicroscopy. Western blots were performed to identify the vascular levels of protein O-linked-N-acetyl-glucosamine (O-GlcNAc) and phosphorylated endothelial NO synthase (eNOS). In arterioles exposed to HG, dilations to histamine were abolished compared to those exposed to NG (max: -6±6% and 69±9%, respectively), while acetylcholine-induced responses were n...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537278</comments>
            <pubDate>Sat, 03 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537278</guid>        </item>
        <item>
            <title>Ethanol induces vascular relaxation via redox-sensitive and nitric oxide-dependent pathways.</title>
            <link>http://www.medworm.com/index.php?rid=5537277&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22155162%26dopt%3DAbstract</link>
            <description>Authors: Rocha JT, Hipólito UV, Callera GE, Yogi A, Filho MD, Bendhack LM, Touyz RM, Tirapelli CR
    Abstract
    We investigated the role of reactive oxygen species (ROS) and nitric oxide (NO) in ethanol-induced relaxation. Vascular reactivity experiments showed that ethanol (0.03-200mmol/L) induced relaxation in endothelium-intact and denuded rat aortic rings isolated from male Wistar rats. Pre-incubation of intact or denuded rings with l-NAME (non selective NOS inhibitor, 100μmol/L), 7-nitroindazole (selective nNOS inhibitor, 100μmol/L), ODQ (selective inhibitor of guanylyl cyclase enzyme, 1μmol/L), glibenclamide (selective blocker of ATP-sensitive K(+) channels, 3μmol/L) and 4-aminopyridine (selective blocker of voltage-dependent K(+) channels, 4-AP, 1mmol/L) reduced ethanol-indu...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537277</comments>
            <pubDate>Sat, 03 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537277</guid>        </item>
        <item>
            <title>Arachidonic acid inhibits Na(+)-K(+)-ATPase via cytochrome P-450, lipooxygenase and protein kinase C-dependent pathways in sheep pulmonary artery.</title>
            <link>http://www.medworm.com/index.php?rid=5537275&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22155164%26dopt%3DAbstract</link>
            <description>In conclusion, the results suggest that 20-HETE, a cytochrome P-450 metabolite of arachidonic acid has a predominant role in the inhibition of functional Na(+)-K(+)-ATPase activity in the sheep pulmonary artery, while the lipooxygenase pathway has a secondary role. It is also evident that protein kinase C is involved in the inhibition of Na(+)-K(+)-ATPase by arachidonic acid/20-HETE in sheep pulmonary artery.
    PMID: 22155164 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537275</comments>
            <pubDate>Sat, 03 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537275</guid>        </item>
        <item>
            <title>Clitocybin B inhibits rat aortic smooth muscle cell proliferation through suppressing PDGF-Rβ phosphorylation.</title>
            <link>http://www.medworm.com/index.php?rid=5537273&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22166585%26dopt%3DAbstract</link>
            <description>Authors: Yoo KD, Park ES, Lim Y, Kang SI, Yoo SH, Won HH, Kim YH, Yoo ID, Yoo HS, Hong JT, Yun YP
    Abstract
    The increased proliferation of vascular smooth muscle cells (VSMCs) in the arterial wall is a critical pathogenic factor for vascular diseases such as atherosclerosis and restenosis after angioplasty. Clitocybin B was reported to have either a potent free radical scavenging effect or effects that were isolated from the culture broth of mushroom Clitocybe aurantiaca. The present study was designed to investigate the effects of clitocybin B on VSMC proliferation and its possible molecular mechanism. Clitocybin B significantly inhibited the proliferation and the DNA synthesis of PDGF-BB-stimulated VSMCs in a concentration-dependent manner. In agreement with these findings, clitoc...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537273</comments>
            <pubDate>Sat, 03 Dec 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537273</guid>        </item>
        <item>
            <title>Resveratrol reverses monocrotaline-induced pulmonary vascular and cardiac dysfunction: A potential role for atrogin-1 in smooth muscle.</title>
            <link>http://www.medworm.com/index.php?rid=5537279&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22146233%26dopt%3DAbstract</link>
            <description>Authors: Paffett ML, Lucas SN, Campen MJ
    Abstract
    Arterial remodeling contributes to elevated pulmonary artery (PA) pressures and right ventricular hypertrophy seen in pulmonary hypertension (PH). Resveratrol, a sirtuin-1 (SIRT1) pathway activator, can prevent the development of PH in a commonly used animal model, but it is unclear whether it can reverse established PH pathophysiology. Furthermore, atrophic ubiquitin ligases, such as atrogin-1 and MuRF-1, are known to be induced by SIRT1 activators but have not been characterized in hypertrophic vascular disease. Therefore, we hypothesized that monocrotaline (MCT)-induced PH would attenuate atrophy pathways in the PA while, conversely, SIRT1 activation (resveratrol) would reverse indices of PH and restore atrophic gene expression. ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5537279</comments>
            <pubDate>Fri, 25 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5537279</guid>        </item>
        <item>
            <title>Linking immunity to atherosclerosis: Implications for vascular pharmacology - A tribute to Göran K. Hansson.</title>
            <link>http://www.medworm.com/index.php?rid=5459906&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22120836%26dopt%3DAbstract</link>
            <description>Authors: Geng YJ, Jonasson L
    Abstract
    For the past decade, we have deepened our understanding of the pathogenesis of atherosclerosis, a chronic arterial disease that causes cardiac and cerebral infarction and peripheral vascular disorders. Because of this extended understanding, more effective strategies for prevention and treatment of this disease are emerging. One of the fundamental mechanisms that lead to progress or regression in atherosclerosis, thus influencing its life-threatening complications, occurs through functional changes in vascular immunity and inflammation. This review briefly summarizes the discoveries in basic and translational sciences in this area and recent advances in clinical medicine against atherosclerotic vascular diseases.
    PMID: 22120836 [PubMed - as...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5459906</comments>
            <pubDate>Sun, 20 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5459906</guid>        </item>
        <item>
            <title>The effect of simvastatin on asymmetric dimethylarginine and flow-mediated vasodilation after optimizing the LDL level - A randomized, placebo-controlled study.</title>
            <link>http://www.medworm.com/index.php?rid=5459907&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22108444%26dopt%3DAbstract</link>
            <description>In conclusion, in cases with optimized LDL-target levels (patients on 80mg Simvastatin), the baseline level of ADMA appears to be a major modulator of %FMD-changes.
    PMID: 22108444 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5459907</comments>
            <pubDate>Sun, 13 Nov 2011 05:00:00 +0100</pubDate>
            <guid isPermaLink="false">5459907</guid>        </item>
        <item>
            <title>Taxol alleviates 2-methoxyestradiol-induced endothelial permeability.</title>
            <link>http://www.medworm.com/index.php?rid=5426232&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22074808%26dopt%3DAbstract</link>
            <description>Authors: Gorshkov BA, Zemskova MA, Verin AD, Bogatcheva NV
    Abstract
    We have previously shown that the anti-cancer agent 2-methoxyestradiol (2ME) induces hyperpermeability across endothelial monolayers. Here, we show that both microtubule disruptor, 2ME, and microtubule stabilizer, paclitaxel (taxol), increase vascular lung permeability in vitro and in vivo. Simultaneous application of 2ME and taxol alleviates 2ME-induced endothelial barrier dysfunction, which is evident by the decreased Evans Blue Dye accumulation in lung tissue and increased transendothelial resistance across monolayers. 2ME significantly increases the level of p38 and MLC phosphorylation in both endothelial monolayers and murine lungs; this increase is suppressed in the presence of taxol. Taxol treatment leads to...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426232</comments>
            <pubDate>Sun, 30 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426232</guid>        </item>
        <item>
            <title>AMP-activated protein kinase and the control of smooth muscle cell hyperproliferation in vascular disease.</title>
            <link>http://www.medworm.com/index.php?rid=5426231&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22074809%26dopt%3DAbstract</link>
            <description>Authors: Ferri N
    Abstract
    Smooth muscle cell (SMC) accumulation within the arterial intima contributes to the formation of atherosclerotic lesions. Emerging data indicate that the adenosine monophosphate-activated protein kinase (AMPK) is a potent inhibitor of SMC proliferation. The anti-proliferative action of AMPK is mediated through multiple mechanisms, including the regulation of cyclin dependent kinase expression p21(Cip1) and p27(kip1) and the inhibition of the mammalian target of rapamycin complex 1 (mTORC1). A favorable effect of AMPK activation on intima hyperplasia has been demonstrated in in vivo experimental models by using the AMPK activator 5-aminoimidazole-4-carboxamide ribonucleoside (AICAR), or by studying the AMPKα(-/-) mice. Starting from these evidences, a numb...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5426231</comments>
            <pubDate>Sun, 30 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5426231</guid>        </item>
        <item>
            <title>MicroRNAs in vascular biology, an introduction to the Vascular Pharmacology Special Issue on microRNAs.</title>
            <link>http://www.medworm.com/index.php?rid=5382616&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22041190%26dopt%3DAbstract</link>
            <description>Authors: Emanueli C
    PMID: 22041190 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382616</comments>
            <pubDate>Wed, 26 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382616</guid>        </item>
        <item>
            <title>Inhibition of Mitogen Activated Protein Kinase Activated Protein Kinase II with MMI-0100 reduces intimal hyperplasia ex vivo and in vivo.</title>
            <link>http://www.medworm.com/index.php?rid=5382617&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D22024359%26dopt%3DAbstract</link>
            <description>Authors: Muto A, Panitch A, Kim N, Park K, Komalavilas P, Brophy CM, Dardik A
    Abstract
    Vein graft intimal hyperplasia remains the leading cause of graft failure, despite many pharmacological approaches that have failed to translate to human therapy. We investigated whether local suppression of inflammation and fibrosis with MMI-0100, a novel peptide inhibitor of Mitogen Activated Protein Kinase Activated Protein Kinase II (MK2), would be an alternative strategy to reduce cell proliferation and intimal hyperplasia. The cell permeable peptide MMI-0100 was synthesized using standard Fmoc chemistry. Pharmacological doses of MMI-0100 induced minimal human endothelial and smooth muscle cell proliferation (30% and 12% respectively). MMI-0100 suppressed IL-6 expression to control levels, w...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5382617</comments>
            <pubDate>Mon, 17 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5382617</guid>        </item>
        <item>
            <title>An in vitro reconstitution system to address the mechanism of the vascular expression of the bradykinin B(1) receptor in response to angiotensin converting enzyme inhibition.</title>
            <link>http://www.medworm.com/index.php?rid=5331882&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21986309%26dopt%3DAbstract</link>
            <description>Authors: Roy C, Marceau E, Gera L, Marceau F
    Abstract
    The expression of the bradykinin (BK) B(1) receptor (B(1)R), lacking in normal vascular tissues, is induced following innate immune system activation and chronic blockade of angiotensin converting enzyme (ACE). To identify cytokine-dependent or -independent mechanisms for the latter phenomenon, the ACE inhibitor enalaprilat and several peptides potentiated in vivo by ACE blockade were applied either directly to human umbilical artery smooth muscle cells (hUA-SMCs) or to differentiated monoblastoid U937 cells to produce a conditioned medium (CM) that was later transferred to hUA-SMCs. A phagocyte stimulant, lipopolysaccharide, did not upregulate B(1)R, measured using [(3)H]Lys-des-Arg(9)-BK binding, or translocate NF-κB to the n...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5331882</comments>
            <pubDate>Sun, 02 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5331882</guid>        </item>
        <item>
            <title>Fraud in biomedical research - The role of journal Editors.</title>
            <link>http://www.medworm.com/index.php?rid=5331883&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21983415%26dopt%3DAbstract</link>
            <description>Authors: De Caterina R, Griffoen AW, Porreca F
    PMID: 21983415 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5331883</comments>
            <pubDate>Sat, 01 Oct 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5331883</guid>        </item>
        <item>
            <title>Biomarkers of endothelial cell activation: Candidate markers for drug-induced vasculitis in patients or drug-induced vascular injury in animals.</title>
            <link>http://www.medworm.com/index.php?rid=5331884&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21968053%26dopt%3DAbstract</link>
            <description>Authors: Zhang J, Hanig JP, De Felice AF
    Abstract
    There is a pressing need for vascular biomarkers for studies of drug-induced vasculitis in patients and drug-induced vascular injury (DIVI) in animals. We previously reviewed a variety of candidate biomarkers of endothelial cell (EC) activation (Zhang et al., 2010). Now we update information on EC activation biomarkers from animal data on DIVI and clinical data of vasculitic patients, particularly patients with primary antineutrophil cytoplasmic autoantibody (ANCA)-associated small vessel vasculitis (primary AAVs), including Wegener's granulomatosis, microscopic polyangiitis, Churg-Strauss syndrome and necrotizing crescentic glomerulonephritis. Drug-associated ANCA-positive small vessel vasculitis (drug-AAVs) can closely resemble pr...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5331884</comments>
            <pubDate>Sat, 24 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5331884</guid>        </item>
        <item>
            <title>Age-related β-adrenergic receptor-mediated vasorelaxation is changed by altering G protein receptor kinase 2 expression.</title>
            <link>http://www.medworm.com/index.php?rid=5266304&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21951806%26dopt%3DAbstract</link>
            <description>In this study we validated that carotid arteries have similar age-related changes in the β-AR signaling axis as aorta. This finding allowed use of in vivo infection and delivery of two adenovirus vectors to carotid arteries of 2-month-old (2M) and 12-month-old (12M) male Fischer 344 rats. Adeno-GRK2 was used to overexpress GRK2, and adeno-β-ARK-ct was used to inhibit GRK2 function. Following a five-day infection, vessels were collected and ex vivo tissue bath was used to evaluate vasoreactivity. We used KCl contracted segments, and determined that overexpression of GRK2 significantly impaired isoproterenol (ISO)-mediated vasorelaxation in both age groups. Maximum relaxation (MAX) to ISO in vessels from 2M decreased from 44% to 21%. MAX to ISO in vessels from 12M decreased from 12% to 6%....</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5266304</comments>
            <pubDate>Sat, 17 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5266304</guid>        </item>
        <item>
            <title>&quot;Fishing&quot; for endothelial microRNA functions and dysfunction.</title>
            <link>http://www.medworm.com/index.php?rid=5249577&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21924380%26dopt%3DAbstract</link>
            <description>&quot;Fishing&quot; for endothelial microRNA functions and dysfunction.
    Vascul Pharmacol. 2011 Sep 8;
    Authors: Santoro MM
    Abstract
    MicroRNAs (e.g. miRNAs), endogenously expressed small non-coding RNAs, control gene expression by regulating target messenger RNA at post-transcriptional level. Recent studies have identified a specific role for microRNAs as key regulators of vascular function and dysfunction. The zebrafish (Danio rerio) system is a useful model system to study endothelial cell homeostasis during normal and pathological conditions. In this review, we describe how the zebrafish model is becoming a useful tool to study the role of microRNAs and their target genes in endothelial and smooth muscle cells both in normal and pathological conditions. Finally, we also discuss the ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5249577</comments>
            <pubDate>Thu, 08 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5249577</guid>        </item>
        <item>
            <title>WITHDRAWN: Retraction notice to &quot;Pigment epithelium-derived factor inhibits vascular endothelial growth factor-and interleukin-1beta-induced vascular permeability and angiogenesis in retinal endothelial cells&quot; Vascular Pharmacology 52 (2010) 84-94.</title>
            <link>http://www.medworm.com/index.php?rid=5221126&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21893214%26dopt%3DAbstract</link>
            <description>This article has been withdrawn at the request of the author(s) and/or editor. The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at http://www.elsevier.com/locate/withdrawalpolicy.
    PMID: 21893214 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221126</comments>
            <pubDate>Fri, 02 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221126</guid>        </item>
        <item>
            <title>All-trans retinoic acid can regulate the expressions of gelatinases and apolipoprotein E in glomerulosclerosis rats.</title>
            <link>http://www.medworm.com/index.php?rid=5221125&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21907828%26dopt%3DAbstract</link>
            <description>In conclusion, gelatinases are associated with apoE expression, and ATRA can increase the gelatinases expressions and reduce the accumulation of apoE in glomerulus of GS rats, but the detailed mechanism needs to be elucidated in the future.
    PMID: 21907828 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5221125</comments>
            <pubDate>Fri, 02 Sep 2011 04:00:00 +0100</pubDate>
            <guid isPermaLink="false">5221125</guid>        </item>
        <item>
            <title>Arterial remodeling and atherosclerosis: miRNAs involvement.</title>
            <link>http://www.medworm.com/index.php?rid=5160090&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21864716%26dopt%3DAbstract</link>
            <description>Authors: Quintavalle M, Condorelli G, Elia L
    Abstract
    Cardiometabolic diseases (CMD) (such as atherosclerosis, diabetes, and hypertension) are the primary cause of death and disability in the Western world. Although lifestyle programs and therapeutic approaches have significantly reduced the socio-economic burden of CMD, a large number of events still cannot be avoided (the so called residual risk). Recent developments in genetics and genomics provide a platform for investigating further this area with the aim of deepening our understanding of the atherosclerotic phenomena underlying CMD, for instance by providing better information on the type of subjects who would benefit the most from therapeutic interventions, or by discovering new genetic and metabolic derangements that may be...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5160090</comments>
            <pubDate>Mon, 15 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5160090</guid>        </item>
        <item>
            <title>Fenofibrate attenuates nicotine-induced vascular endothelial dysfunction in the rat.</title>
            <link>http://www.medworm.com/index.php?rid=5160089&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21864717%26dopt%3DAbstract</link>
            <description>Authors: Chakkarwar VA
    Abstract
    The study has been designed to investigate the effect of fenofibrate in nicotine-induced vascular endothelial dysfunction (VED) in rats. Nicotine (2mg/kg/day, i.p., 4weeks) was administered to produce VED in rats. The development of VED was assessed by employing isolated aortic ring preparation and estimating serum and aortic concentration of nitrite/nitrate. Further, the integrity of vascular endothelium was assessed using the scanning electron microscopy of thoracic aorta. The expression of mRNA for p22phox and eNOS was assessed by using reverse transcriptase-polymerase chain reaction. Serum thiobarbituric acid reactive substances concentration (TBARS) and aortic superoxide anion concentration were estimated to assess oxidative stress. Moreover, th...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5160089</comments>
            <pubDate>Mon, 15 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5160089</guid>        </item>
        <item>
            <title>MicroRNAs regulating cell pluripotency and vascular differentiation.</title>
            <link>http://www.medworm.com/index.php?rid=5160091&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21854874%26dopt%3DAbstract</link>
            <description>Authors: Howard L, Kane NM, Milligan G, Baker AH
    Abstract
    Human embryonic stem cells (hESC) offer broad potential for regenerative medicine owing to their capacity for self renewal, exponential scale up and differentiation into any cell type in the adult body. hESC have been proposed as a potentially unlimited source for the generation of transplantable, healthy, functional vascular cells for repair of ischemic tissues. To optimally harness this potential necessitates precise control over biological processes that govern maintenance, pluripotency and cell differentiation including signalling cascades, gene expression profiles and epigenetic modification. Such control may be elicited by microRNAs, which are powerful negative regulators of gene expression. Here, we review the role fo...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5160091</comments>
            <pubDate>Wed, 10 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5160091</guid>        </item>
        <item>
            <title>microRNAs as peripheral blood biomarkers of cardiovascular disease.</title>
            <link>http://www.medworm.com/index.php?rid=5142446&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21846509%26dopt%3DAbstract</link>
            <description>Authors: Di Stefano V, Zaccagnini G, Capogrossi MC, Martelli F
    Abstract
    A host of studies have established essential roles for microRNAs in cardiovascular development and disease. Moreover, the discovery of stable microRNAs in bodily fluids indicated their potential as non-invasive biomarkers. In this review, we summarize the current studies describing microRNAs in blood cells or serum/plasma, as potential biomarkers of cardiovascular disease.
    PMID: 21846509 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5142446</comments>
            <pubDate>Fri, 05 Aug 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5142446</guid>        </item>
        <item>
            <title>&quot;ApoptomiRs&quot; in vascular cells: Their role in physiological and pathological angiogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5108283&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21798370%26dopt%3DAbstract</link>
            <description>&quot;ApoptomiRs&quot; in vascular cells: Their role in physiological and pathological angiogenesis.
    Vascul Pharmacol. 2011 Jul 27;
    Authors: Quintavalle C, Garofalo M, Croce CM, Condorelli G
    MicroRNAs (miRNAs) have emerged as crucial players regulating the magnitude of gene expression in a variety of organisms. This class of short (22 nucleotides) noncoding RNA molecules have been shown to participate in almost every cellular process investigated so far, and their deregulation is observed in different human pathologies including cancer, heart disease, and neurodegeneration. These new molecular regulators have been identified also in endothelial cells (ECs), and their role in the regulation of different aspects of the angiogenic process has been recently investigated in a variety of labor...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5108283</comments>
            <pubDate>Tue, 26 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5108283</guid>        </item>
        <item>
            <title>MicroRNAs and vascular (dys)function.</title>
            <link>http://www.medworm.com/index.php?rid=5108281&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21802526%26dopt%3DAbstract</link>
            <description>Authors: Hartmann D, Thum T
    MicroRNAs (miRNAs) are small non-coding RNAs, that control diverse cellular functions by either promoting degradation or inhibition of target messenger RNA translation. An aberrant expression profile of miRNAs has been linked to human diseases, including cardiovascular dysfunctions. This review summarizes the latest insights in the identification of vascular-specific miRNAs and their targets, as well as their roles and mechanisms in the vasculature. Furthermore, we discuss how manipulation of these miRNAs could represent a novel therapeutic approach in the treatment of vascular dysfunction.
    PMID: 21802526 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5108281</comments>
            <pubDate>Fri, 22 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5108281</guid>        </item>
        <item>
            <title>Reduced placental vascular reactivity to 5-hydroxytryptamine in pre-eclampsia and the status of 5HT(2A) receptors.</title>
            <link>http://www.medworm.com/index.php?rid=5108279&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21803171%26dopt%3DAbstract</link>
            <description>This study investigates the contractile response to 5 hydroxytryptamine (5HT) of chorionic artery and vein segments from normotensive (NT) and pre-eclamptic (PE) placentae. It also looked at the effectiveness of ketanserin (KET), a 5HT(2A) receptor antagonist, in reducing 5HT-mediated vasoconstriction. 5HT induced vasoconstriction in all of the vessels was studied. Compared to NT vessels, Emax (%KCl) was significantly reduced in PE arteries (p&amp;lt;0.05) and veins (p&amp;lt;0.0005). The mean Emax for NT arteries was 104.1 (±10.71) whilst PE arteries showed a mean Emax of 57.02 (±12.13). KET produced a statistically significant reduction of Emax in both vessels in NT and the arteries in PE. However the antagonistic effect of KET was not pronounced in PE veins. The EC50 values for NT and PE arte...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5108279</comments>
            <pubDate>Fri, 22 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5108279</guid>        </item>
        <item>
            <title>Tyrosine kinase inhibitor, genistein, reduces renal inflammation and injury in streptozotocin-induced diabetic mice.</title>
            <link>http://www.medworm.com/index.php?rid=5108277&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21807121%26dopt%3DAbstract</link>
            <description>Authors: Elmarakby AA, Ibrahim AS, Faulkner J, Mozaffari MS, Liou GI, Abdelsayed R
    Tyrosine kinase inhibition is known to reduce diabetes-induced end-organ damage but the mechanisms remain elusive. We hypothesized that inhibition of tyrosine kinase reduces renal inflammation and injury in streptozotocin-induced diabetes. Male C57BL/6 mice were given daily injections of streptozotocin (45mg/kg/day, i.p. for 5days); control animals received the vehicle (citrate buffer). Thereafter, streptozotocin-treated mice were treated with genistein (10mg/kg, i.p three times a week for 10weeks, n=8-10/group) or the vehicle (5% DMSO). The streptozotocin-treated mice displayed significant elevation in blood glucose level and decrease in plasma insulin level compared to their vehicle-treated controls. T...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5108277</comments>
            <pubDate>Fri, 22 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5108277</guid>        </item>
        <item>
            <title>Trichostatin a prevents neointimal hyperplasia via activation of Krüppel like factor 4.</title>
            <link>http://www.medworm.com/index.php?rid=5064563&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21763782%26dopt%3DAbstract</link>
            <description>In this study, we investigated the effect and mechanism whereby TSA prevents the proliferation of VSMCs and neointimal hyperplasia induced by balloon injury in rat carotid artery. Local administration of TSA significantly prevented neointimal hyperplasia. TSA dramatically inhibited the proliferation and DNA synthesis of VSMCs in response to FBS or PDGF-BB. Overexpression of Krüppel like factor 4 (KLF4) blocked the cell proliferation and DNA synthesis, as determined by the MTT and [(3)H]thymidine incorporation assays, whereas knockdown of KLF4 resulted in an increase in VSMC proliferation. In VSMCs, TSA increased the mRNA level and protein expression of KLF4. Treatment with TSA or transfection of KLF4 increased the expression of both p21 and p27 and promoter activity. In addition, the anti...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5064563</comments>
            <pubDate>Wed, 13 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5064563</guid>        </item>
        <item>
            <title>MicroRNA regulation in angiogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=5064561&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21777698%26dopt%3DAbstract</link>
            <description>Authors: Caporali A, Emanueli C
    The term angiogenesis derives from the Greek words 'angeio' meaning blood vessel, and 'genesis' meaning production or birth, together referring to the creation of blood vessels within the body. This term has been used to generally indicate the growth and remodeling process of the primitive vascular network into a complex network during pre-natal development. After birth, reparative angiogenesis is activated during wound healing and in response to ischemia, while pathological angiogenesis contributes to tumor growth and metastasis, arthritis and ocular diseases, such as diabetic retinopathy. MicroRNAs (miRNAs) are a class of endogenous, small, non-coding RNAs that control gene expression by acting on target mRNAs for promoting either their degradation or ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5064561</comments>
            <pubDate>Wed, 13 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5064561</guid>        </item>
        <item>
            <title>ZLJ-6, a novel COX/5-LOX inhibitor, attenuates TNF-α-induced endothelial E-selectin, ICAM-1 and VCAM-1 expression and monocyte-endothelial interactions via a COX/5-LOX-independent mechanism.</title>
            <link>http://www.medworm.com/index.php?rid=5064562&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21777697%26dopt%3DAbstract</link>
            <description>Authors: Chen L, Zhao Q, Wang XL, You R, Zhang YH, Ji H, Lai YS
    Nonsteroidal anti-inflammatory drugs (NSAIDs) are previously found to possess prostaglandin and leukotriene-independent anti-inflammatory effect. The aim of the present study was to investigate the prostaglandin and leukotriene-independent anti-inflammatory effect of an imidazolone COX/5-LOX inhibitor ZLJ-6 and the underlying mechanism. Pretreatment human umbilical vein endothelial cells (HUVECs) with ZLJ-6 (3, 10 and 30μM) concentration-dependently decreased TNF-α-induced monocyte-endothelial interactions in both static and dynamic conditions whereas no effect was found after pretreatment with the COX-2 inhibitor celecoxib (30μM), 5-LOX inhibitor zileuton (30μM) and the combination of them. ZLJ-6 also attenuated expre...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5064562</comments>
            <pubDate>Mon, 11 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5064562</guid>        </item>
        <item>
            <title>Glutathione peroxidase-deficient smooth muscle cells cause paracrine activation of normal smooth muscle cells via cyclophilin A.</title>
            <link>http://www.medworm.com/index.php?rid=5064474&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21782974%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: Reduction in vascular cell GPx1 activity and the associated increase in oxidative stress cause CyPA-mediated paracrine activation of SMCs. These findings identify a novel mechanism by which an imbalance in antioxidant capacity may contribute to vascular disease.
    PMID: 21782974 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5064474</comments>
            <pubDate>Mon, 11 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5064474</guid>        </item>
        <item>
            <title>Vasodilatation produced by Fasudil Mesylate in vivo and in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=5064564&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21763460%26dopt%3DAbstract</link>
            <description>Authors: Li Q, Chen Y, Sun L, Fu G, Guo L
    To investigate the vasorelaxant effect of fasudil mesylate (FM) in vivo and in vitro. The relaxation effect of FM was studied using cerebral vasospasm (CVS) model in vivo and isolated aortic rings in vitro. FM (0.35, 1.2, 3.5mg·kg(-1)) increased cerebrovascular flow (CVF) and femoral blood flow (FBF) dose-dependently in vivo, however, the relaxation effects of FM on cerebral vessels were much stronger than on peripheral vessels; FM showed dose-dependent relaxation of isolated aortic rings contracted by Methoxamine (Met) or KCl in vitro. The relaxation IC(50) of FM and Prasozin (Pra) to the rabbit aortic rings contracted by Met are 27.54μM and 0.01μM respectively, and the relaxation IC(50) of FM to the rabbit and rat aortic rings contracted b...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5064564</comments>
            <pubDate>Tue, 05 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5064564</guid>        </item>
        <item>
            <title>The G protein-coupled estrogen receptor GPER/GPR30 as a regulator of cardiovascular function.</title>
            <link>http://www.medworm.com/index.php?rid=5064568&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21742056%26dopt%3DAbstract</link>
            <description>Authors: Meyer MR, Prossnitz ER, Barton M
    Endogenous estrogens are important regulators of cardiovascular homeostasis in premenopausal women and delay the development of hypertension and coronary artery disease. These hormones act via three different estrogen receptors affecting both gene transcription and rapid signaling pathways in a complex interplay. In addition to the classical estrogen receptors ERα and ERβ, which are known mediators of estrogen-dependent vascular effects, a G protein-coupled estrogen receptor termed GPER that is expressed in the cardiovascular system has recently been identified. Endogenous human 17β-estradiol, selective estrogen receptor modulators (SERMs) including tamoxifen and raloxifene, and selective estrogen receptor downregulators (SERDs) such as ICI ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5064568</comments>
            <pubDate>Mon, 04 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5064568</guid>        </item>
        <item>
            <title>Pharmacological and expression profile of the prostaglandin I(2) receptor in the rat craniovascular system.</title>
            <link>http://www.medworm.com/index.php?rid=5064566&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21749934%26dopt%3DAbstract</link>
            <description>This study investigates the functional and molecular characteristics of the IP receptor in the rat craniovascular system. In the closed cranial window model, iloprost, an IP receptor agonist, dilated the rat middle meningeal artery (MMA) (E(max)=170%±16%; pED(50)=6.5±0.2) but not the rat cerebral artery (CA) in vivo. The specific antagonist of the IP receptor, CAY10441, significantly blocked the iloprost-induced response dose-dependently, with the highest dose attenuating iloprost (1μgkg(-1)) induced dilatations by 70% (p&amp;lt;0.05). CAY10441 did not have any effect on the prostaglandin E(2)-induced vasodilatory response, thus suggesting no interaction with EP(2) and EP(4) receptors. IP receptor mRNA transcripts and protein were present in meningeal as well as in cerebral rat vasculature,...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5064566</comments>
            <pubDate>Mon, 04 Jul 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5064566</guid>        </item>
        <item>
            <title>Nifedipine inhibits vascular smooth muscle cell proliferation and reactive oxygen species production through AMP-activated protein kinase signaling pathway.</title>
            <link>http://www.medworm.com/index.php?rid=5011932&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21708289%26dopt%3DAbstract</link>
            <description>Authors: Sung JY, Choi HC
    The dihydropyridine calcium channel blocker nifedipine induces specific pharmacological effects by binding to L-type calcium channels, which results in a reduced calcium influx in vascular smooth muscle cells (VSMCs) and is currently employed in antihypertensive drug. Dihydropyridine calcium channel blocker is reported to reduce oxidative stress and exhibits anti-proliferative effect in VSMCs. VSMCs are useful in the study of atherosclerosis because they show cell proliferation and reactive oxygen species (ROS) production with growth factor. To determine the mechanisms involved in these effects, we investigated the influence of nifedipine-induced AMP-activated protein kinase (AMPK) activation on VSMC proliferation and ROS production by using rat aortic VSMCs i...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=5011932</comments>
            <pubDate>Fri, 24 Jun 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">5011932</guid>        </item>
        <item>
            <title>Cardiovascular effects of DPP-4 inhibition: Beyond GLP-1.</title>
            <link>http://www.medworm.com/index.php?rid=4968998&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21664294%26dopt%3DAbstract</link>
            <description>Authors: Fadini GP, Avogaro A
    Dipeptydil-peptidase-4 (DPP-4) inhibitors are available as oral anti-hyperglycemic drugs for the treatment of type 2 diabetes. Their metabolic effect is mediated through sparing incretin hormones (such as glucagon-like peptide-1, GLP-1) from the rapid degradation by DPP-4. In turn, GLP-1 improves meal-stimulated insulin secretion by pancreatic β-cells thus reducing hyperglycemia. It has been shown that GLP-1 signaling is also active in the cardiovascular system, where it may exert beneficial effects. However, DPP-4 has several non-incretin substrates, and its immunomodulatory activity is known from decades. DPP-4 physiologically cleaves cytokines, chemokines and neuropeptides involved in inflammation, immunity, and vascular function. Owing to these off-ta...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4968998</comments>
            <pubDate>Mon, 30 May 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4968998</guid>        </item>
        <item>
            <title>Tyrphostin AG490 reduces NAPDH oxidase activity and expression in the aorta of hypercholesterolemic apolipoprotein E-deficient mice.</title>
            <link>http://www.medworm.com/index.php?rid=4822950&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21457788%26dopt%3DAbstract</link>
            <description>Authors: Fenyo IM, Florea IC, Raicu M, Manea A
    Oxidative stress-induced vascular injury represents a major contributor to the pathoetiology of atherosclerosis. Elevated NADPH oxidase (Nox) activity promotes oxidative injury of the cardiovascular cells. Janus-tyrosine-kinase (Jak) family regulate various aspects of the atherosclerotic process e.g., inflammation, cellular growth, proliferation, and migration. Here, we investigated the potential of Jak2 inhibition to counteract Nox-dependent O(2)(•-) formation in atherogenesis in hypercholesterolemic apolipoprotein E-deficient (ApoE(-/-)) mice. Male ApoE(-/-) mice fed a high-fat, cholesterol-rich diet were treated for 5weeks with either vehicle or tyrphostin AG490 (1mg/kg), a specific Jak2 inhibitor. Lucigenin-enhanced-chemiluminescence...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4822950</comments>
            <pubDate>Tue, 29 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4822950</guid>        </item>
        <item>
            <title>Cellular and molecular mechanisms of vascular injury in diabetes - Part II: Cellular mechanisms and therapeutic targets.</title>
            <link>http://www.medworm.com/index.php?rid=4822952&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21453785%26dopt%3DAbstract</link>
            <description>Authors: Madonna R, De Caterina R
    Although the mechanisms by which insulin-resistance and hyperglycemia lead to cardiovascular disease are still incompletely understood, all mechanisms apparently converge on the vessel wall and the endothelium as a common disease target. Endothelial cells play a crucial role in vascular homeostasis, providing a functional barrier and modulating several signals involved in vasomotion, as well as antiplatelet, anti-inflammatory, anti-proliferative, and anti-oxidant properties of the vessel wall. Endothelial cell dysfunction occurs early in diabetes and insulin resistance states. Since atherosclerosis may result from an imbalance between the magnitude of vascular injury and the capacity of repair, a role has been recently postulated for a defective mobili...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4822952</comments>
            <pubDate>Mon, 28 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4822952</guid>        </item>
        <item>
            <title>Cellular and molecular mechanisms of vascular injury in diabetes - Part I: Pathways of vascular disease in diabetes.</title>
            <link>http://www.medworm.com/index.php?rid=4822951&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21453786%26dopt%3DAbstract</link>
            <description>Authors: Madonna R, De Caterina R
    Diabetes-induced micro- and macrovascular complications are the major causes of morbidity and mortality in diabetic patients. While hyperglycemia is a key factor for the pathogenesis of diabetic microvascular complications, it is only one of the multiple factors capable of increasing the risk of macrovascular complications. Hyperglycemia induces vascular damage probably through a single common pathway - increased intracellular oxidative stress - linking four major mechanisms, namely the polyol pathway, advanced glycation end-products (AGEs) formation, the protein kinase C (PKC)-diacylglycerol (DAG) and the hexosamine pathways. In addition, in conditions of insulin resistance, i.e., preceding the onset of type 2 diabetes, the phosphatidylinositol (PI) 3...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4822951</comments>
            <pubDate>Mon, 28 Mar 2011 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4822951</guid>        </item>
        <item>
            <title>Statins as modulators of colon cancer cells induced cytokine secretion by human PBMC.</title>
            <link>http://www.medworm.com/index.php?rid=4662886&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21440087%26dopt%3DAbstract</link>
            <description>Authors: Bergman M, Salman H, Djaldetti M, Bessler H
    The study was designed to examine whether the hydrophilic statin - pravastatin and the hydrophobic statin - simvastatin affect colon cancer cell-induced cytokine secretion by peripheral blood mononuclear cells (PBMC). Statins were added to human colon cancer cells (HT-29 and RKO), or to PBMC incubated separately or jointly. The secretion of the pro-inflammatory cytokines IL-1β and IFNγ and that of the anti-inflammatory cytokines IL-1ra and IL-10 induced by cancer cells was decreased by simvastatin but not by pravastatin, whereas that of IL-6 was not affected by both drugs. Conditioned media from colon cancer cells incubated with either simvastatin or pravastatin induced stimulation of cytokine production by PBMC similar to that cau...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4662886</comments>
            <pubDate>Sat, 26 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4662886</guid>        </item>
        <item>
            <title>The Annexin A2 System and Vascular Homeostasis.</title>
            <link>http://www.medworm.com/index.php?rid=4662885&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21440088%26dopt%3DAbstract</link>
            <description>Authors: Flood EC, Hajjar KA
    Optimal fibrin balance requires precisely controlled plasmin generation on the surface of endothelial cells, which line the blood vessel wall. As a co-receptor for plasminogen and tissue plasminogen activator (tPA), which are key factors in plasmin generation, the annexin A2 (A2) complex promotes vascular fibrinolysis. The intracellular A2 complex is a heterotetramer of two A2 monomers and two copies of the associated protein, p11. In response to endothelial cell activation, A2 is phosphorylated by src-kinase, and translocated to the cell surface in a highly regulated manner. Over- expression of A2 is seen in acute promyelocytic leukemia during the early hemorrhagic phase, while high titer antibodies to A2, as in antiphospholipid syndrome or cerebral venous...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4662885</comments>
            <pubDate>Wed, 23 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4662885</guid>        </item>
        <item>
            <title>Cholesterol induces apoptosis-associated loss of the activated leukocyte cell adhesion molecule (ALCAM) in human monocytes.</title>
            <link>http://www.medworm.com/index.php?rid=4662884&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21440089%26dopt%3DAbstract</link>
            <description>In conclusion, cholesterol-induced apoptosis in monocytes is accompanied by reduced expression of ALCAM and attenuated monocyte migration. This may restrain monocytes at cholesterol-rich sites and thereby expedite vascular lesion formation.
    PMID: 21440089 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4662884</comments>
            <pubDate>Wed, 23 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4662884</guid>        </item>
        <item>
            <title>Acute DPP-4 inhibition modulates vascular tone through GLP-1 independent pathways.</title>
            <link>http://www.medworm.com/index.php?rid=4602421&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21397040%26dopt%3DAbstract</link>
            <description>The objective of this study was to examine the acute effects of DPP-4 inhibition on vascular responses and to study the underlying mechanisms of alteration in tone. Aortic segments from C57BL/6 mice were treated with vasoconstrictors and exposed to various doses of alogliptin, a selective DPP-4 inhibitor. Vasodilator responses were evaluated using pathway specific antagonists to elucidate mechanisms of response. In parallel experiments, cultured human umbilical vein endothelial cells (HUVEC) were exposed to varying concentrations of alogliptin to evaluate the effects on candidate vasodilator pathways. Alogliptin relaxed phenylephrine and U46619 pre-constricted aortic segments in a dose dependent manner. Relaxation responses were not affected by the glucagon-like peptide-1 (GLP-1) receptor ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4602421</comments>
            <pubDate>Wed, 09 Mar 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4602421</guid>        </item>
        <item>
            <title>Mechanism of attenuation of diabetes mellitus and hypercholesterolemia induced vascular endothelial dysfunction by protein tyrosine phosphatase inhibition.</title>
            <link>http://www.medworm.com/index.php?rid=4415422&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21237289%26dopt%3DAbstract</link>
            <description>Authors: Sharma S, Singh M, Sharma PL
    The study has been designed to investigate downstream mechanisms in the PTPase inhibition mediated attenuation of diabetes mellitus and hypercholesterolemia-induced vascular endothelial dysfunction. Diabetes mellitus was induced in rats using streptozotocin (55mg/kg, i.v. once), while hypercholesterolemia was produced by feeding high cholesterol diet. After 4weeks of streptozotocin and Cholesterol rich diet administration, vascular endothelium dysfunction was assessed, in terms of attenuation of acetylcholine-induced, endothelium-dependent relaxation (Isolated Aortic Ring Preparation), a decrease in serum nitrate/nitrite level, as well as mRNA expression of eNOS (rtPCR) and disruption of integrity of vascular endothelium (Electron microscopy). Afte...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4415422</comments>
            <pubDate>Thu, 13 Jan 2011 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4415422</guid>        </item>
        <item>
            <title>Total Ginsenosides suppress the neointimal hyperplasia of rat carotid artery induced by balloon injury.</title>
            <link>http://www.medworm.com/index.php?rid=4353678&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21187161%26dopt%3DAbstract</link>
            <description>This study aims to observe the potential effect of total ginsenosides (TG) on the hypertrophic vascular diseases. The model of vascular neointimal hyperplasia was established by rubbing the endothelia of the common carotid artery with a balloon in male Sprague Dawley rats. TG (15mg/kg/day, 45mg/kg/day), L-arginine (L-arg) 200mg/kg/day, and NG-nitro-L-arginine-methyl ester (L-NAME) 100mg/kg/day used with the same dose of L-arg or TG 45mg/kg/day were given for 7 and 14 consecutive days after surgery. TG and L-arg administrations significantly ameliorated the histopathology of injured carotid artery, which was abolished or blunted by L-NAME, an NOS inhibitor; TG and L-arg could also remarkably reduce the expression of proliferating cell nuclear antigen (PCNA), a proliferation marker of vascul...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4353678</comments>
            <pubDate>Sat, 25 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4353678</guid>        </item>
        <item>
            <title>Vascular Pharmacology - New Editorial Board.</title>
            <link>http://www.medworm.com/index.php?rid=4353679&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21185947%26dopt%3DAbstract</link>
            <description>Authors: De Caterina R, Pearson J, Iruela-Arispe L
    
    PMID: 21185947 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4353679</comments>
            <pubDate>Fri, 24 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4353679</guid>        </item>
        <item>
            <title>Prostacyclin, not only nitric oxide, is a mediator of the vasorelaxation induced by acetylcholine in aortas from rats submitted to cecal ligation and perforation (CLP).</title>
            <link>http://www.medworm.com/index.php?rid=4285422&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21167958%26dopt%3DAbstract</link>
            <description>This study aimed to investigate the endothelium-dependent relaxation induced by acetylcholine and the factors involved in this relaxation, using aortic rings isolated from rats submitted to cecal ligation and perforation (CLP), two hours after induction of sepsis, which characterizes the hyperdynamic phase of sepsis. Under inhibition of constitutive NO-synthases (cNOS), the relaxation induced by acetylcholine was greater in the aortic rings of rats submitted to CLP compared with sham-operated rat aortic rings. The cyclooxygenase inhibitor indomethacin normalized this response, and the concentration of the stable metabolite of prostacyclin in the aorta of CLP rats increased in basal conditions and after stimulation with acetylcholine. Acetylcholine-induced NO production was lower in the end...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4285422</comments>
            <pubDate>Wed, 15 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4285422</guid>        </item>
        <item>
            <title>The effect of nebivolol on asymmetric dimethylarginine system in spontaneously hypertension rats.</title>
            <link>http://www.medworm.com/index.php?rid=4285423&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21167314%26dopt%3DAbstract</link>
            <description>In this study SHR and age-matched Wister-Kyoto (WKY) rats were randomly divided into 4 groups：SHR treated with nebivolol(8mg/ kg/day, i.g.); SHR treated with Atenolol(80mg/ kg/day, i.g.); SHR control group; WKY control group. Nebivolol induced an acute and significant reduction in systolic blood pressure in SHR. Compared with WKY, plasma ADMA was elevated significantly, while NOS activity and NO were decreased in SHR. In aorta and mesenteric artery of SHR, the expression of eNOS and DDAH 2 reduced, but expression of PRMT 1 increased. And ROS level in aorta also increased. Nebivolol increased plasma NO and NOS activity, attenuated ADMA level. The expression of eNOS and DDAH 2 were up-regulated, PRMT 1 expression were down-regulated after nebivolol treatment. Nebivolol also reduced aortic ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4285423</comments>
            <pubDate>Tue, 14 Dec 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4285423</guid>        </item>
        <item>
            <title>Lack of Heterologous Receptor Desensitization Induced by Angiotensin II Type 1 Receptor Activation in Isolated Normal Rat Thoracic Aorta.</title>
            <link>http://www.medworm.com/index.php?rid=4224187&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21122823%26dopt%3DAbstract</link>
            <description>In conclusion, angiotensin II induced biphasic responses can be attributed to AT(1) receptors activation and rapid desensitization with time. Desensitization proved to be homologous in nature, since precontractile tone induced by phenylephrine was not depressed by angiotensin II (i.e., angiotensin II did not induce heterologous α(1)-adrenergic receptors desensitization). We found no functional evidence of the participation of AT(2) receptors in angiotensin II elicited biphasic contractions. Angiotensin II does not exert relaxant effects in normal rat aorta.
    PMID: 21122823 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4224187</comments>
            <pubDate>Sun, 28 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4224187</guid>        </item>
        <item>
            <title>Inhibition of vascular endothelial growth factor-induced angiogenesis by scopoletin through interrupting the autophosphorylation of VEGF receptor 2 and its downstream signaling pathways.</title>
            <link>http://www.medworm.com/index.php?rid=4187890&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21078410%26dopt%3DAbstract</link>
            <description>Authors: Pan R, Dai Y, Gao XH, Lu D, Xia YF
    Our previous studies revealed that scopoletin, the main bioactive constituent of Erycibe obtusifolia Benth stems, exerted anti-arthritic activity in vivo partly by preventing synovial angiogenesis. Herein we further investigated the anti-angiogenic potential and related mechanisms of this coumarin compound in vivo and in vitro. On chick chorioallantoic membrane (CAM) model, scopoletin (10, 30, 100nmol/egg) dose-dependently reduced the blood vessels that were quantified by counting the number of blood vessel branch points. In vitro, scopoletin at concentrations above 30μM obviously inhibited the VEGF-induced tube formation, proliferation and migration of human umbilical vein endothelial cells (HUVECs). Furthermore, scopoletin was shown to blo...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4187890</comments>
            <pubDate>Fri, 12 Nov 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4187890</guid>        </item>
        <item>
            <title>Combretastatin-induced hypertension and the consequences for its combination with other therapies.</title>
            <link>http://www.medworm.com/index.php?rid=4140598&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D21040805%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: CA4P significantly increased Hct, [Hb] and MABP. Hypertension, but not increases in Hct and [Hb], could be reversed with the antihypertensive drug HDZ. CA4P significantly improved tumour response to radiation or thermoradiation, neither of which was influenced by the addition of HDZ.
    PMID: 21040805 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4140598</comments>
            <pubDate>Fri, 29 Oct 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">4140598</guid>        </item>
        <item>
            <title>Does atorvastatin induce aortic smooth muscle cell apoptosis in vivo?</title>
            <link>http://www.medworm.com/index.php?rid=4098670&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20951229%26dopt%3DAbstract</link>
            <description>Authors: Doyon M, Hale TM, Huot-Marchand JE, Wu R, de Champlain J, Deblois D
    It has been reported that HMG-CoA reductase inhibitors such as atorvastatin induce vascular smooth muscle (SMC) apoptosis in vitro. However, this effect remains to be demonstrated in vivo. The present studies were designed to test the ability of atorvastatin to induce SMC apoptosis in vivo, using the spontaneously hypertensive rat (SHR) as a well-known reference model of SMC apoptosis induction in vivo by cardiovascular drugs including the calcium channel blocker amlodipine. Atorvastatin was administered to SHR for 3 or 6weeks either alone or together with amlodipine, a drug combination clinically available to patients. Primary endpoints included aortic medial hypertrophy and aortic SMC hyperplasia, internucle...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4098670</comments>
            <pubDate>Tue, 12 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4098670</guid>        </item>
        <item>
            <title>Anti-aggregating effect of bay 58-2667, an activator of soluble guanylyl cyclase.</title>
            <link>http://www.medworm.com/index.php?rid=4066689&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20933607%26dopt%3DAbstract</link>
            <description>Authors: Roger S, Paysant J, Badier-Commander C, Cordi A, Verbeuren TJ, Félétou M
    The purpose of the present study was to determine whether an activator of soluble guanylyl cyclase (sGC), BAY58-2667, inhibits platelet aggregation and to clarify its mechanism of action. Blood was collected from anaesthetized WKY rats. The aggregation of washed platelet was measured and the production of cAMP and cGMP was determined. BAY 58-2667 produced a partial inhibition of the ADP and collagen induced platelet aggregation, but did not significantly affect thrombin-induced aggregation. In ADP-induced platelet aggregation, the inhibitory effects of BAY 58-2667 was associated with an increased level of both cGMP and cAMP while that of the prostacyclin analogue, beraprost, was correlated only with an ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4066689</comments>
            <pubDate>Tue, 05 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4066689</guid>        </item>
        <item>
            <title>Inhibition of TNF-α-induced adhesion molecule expression by diosgenin in mouse vascular smooth muscle cells via downregulation of the MAPK, Akt and NF-κB signaling pathway.</title>
            <link>http://www.medworm.com/index.php?rid=4066690&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20932938%26dopt%3DAbstract</link>
            <description>This study examined the effect of diosgenin on the expression of adhesion molecules induced by TNF-α in cultured mouse VSMC cell line, MOVAS-1. Preincubation of VSMCs for 2h with diosgenin (0.1-10 μM) dose-dependently inhibited TNF-α-induced adhesion of THP-1 monocytic cells and mRNA and protein expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). Diosgenin abrogated TNF-α induced production of intracellular reactive oxygen species (ROS) and phosphorylation of p38, ERK, JNK and Akt. Diosgenin was also shown to inhibit NK-κB activation induced by TNF-α. Furthermore, diosgenin inhibited TNF-α-induced ΙκΒ kinase activation, subsequent degradation of ΙκΒα, and nuclear translocation of NF-κB. Our results indicate that diosgen...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4066690</comments>
            <pubDate>Sun, 03 Oct 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4066690</guid>        </item>
        <item>
            <title>Atherosclerosis Induced by a High-fat Diet Is Alleviated by Lithium Chloride via Reduction of VCAM Expression in ApoE-deficient Mice.</title>
            <link>http://www.medworm.com/index.php?rid=4030516&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20888430%26dopt%3DAbstract</link>
            <description>Authors: Choi SE, Jang HJ, Kang Y, Jung JG, Han SJ, Kim HJ, Kim DJ, Lee KW
    Endothelial cell dysfunction may play an important role in the development of various vascular diseases, including atherosclerosis. Here we investigated whether lithium chloride (LiCl), an inhibitor of glycogen synthase kinase-3Î² (GSK-3 Î²), could counteract atherosclerosis induced by a high-fat diet in ApoE(-/-) mice. Ten-week-old male mice were randomly divided into four groups: normal chow diet, high-fat diet (i.e., 20% fat, 0.5% cholesterol), high-fat diet with LiCl treatment for 6 weeks and high-fat diet with LiCl treatment for 14 weeks. Examination of plasma profiles indicated that blood glucose levels were significantly decreased by LiCl treatment. Supplementation with LiCl dramatically reduced ather...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4030516</comments>
            <pubDate>Tue, 28 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4030516</guid>        </item>
        <item>
            <title>LPS from Porphyromonas gingivalis increases the sensitivity of contractile response mediated by endothelin-B (ET(B)) receptors in cultured endothelium-intact rat coronary arteries.</title>
            <link>http://www.medworm.com/index.php?rid=4030515&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20888431%26dopt%3DAbstract</link>
            <description>Authors: Ghorbani B, Holmstrup P, Edvinsson L, Kristiansen KA, Sheykhzade M
    The purpose of our study was to examine if lipopolysaccharide (LPS) from Porphyromonas gingivalis (P.g.) modifies the vasomotor responses to Endothelin-1 (ET-1) and Sarafotoxin 6c (S6c) in rat coronary arteries. The arteries were studied directly or following organ culture for 24 hrs in absence and presence of 2.5 EU/ml LPS. The contractile responses of coronary arteries were investigated by using the selective ETB receptor agonist S6c (1 pM - 0.3 Î¼M) and ET-1 (1 pM - 0.3 Î¼M). The functional studies demonstrated an augmented contractile response only to S6c in isolated rat coronary arteries after organ culture (with or without LPS). These contractile responses by S6c were blocked by the selective ETB rece...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4030515</comments>
            <pubDate>Tue, 28 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4030515</guid>        </item>
        <item>
            <title>Pulmonary allergic reactions impair systemic vascular relaxation in ragweed sensitive mice.</title>
            <link>http://www.medworm.com/index.php?rid=4030514&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20888432%26dopt%3DAbstract</link>
            <description>In this study, we used a murine model of allergen sensitization in which aspiration of allergen induces pulmonary and systemic inflammation, to test the hypothesis that pulmonary exposure to allergen alters vascular relaxation responses. BALB/C mice were sensitized by intra-peritoneal injection of ragweed and challenged by intratracheal instillation of allergen. Airway hyperreactivity and pulmonary inflammation were confirmed, and endothelium-dependent and -independent reactivity of thoracic aorta rings were evaluated. Ragweed-sensitization and challenge induced airway hyperreactivity to methacholine and pulmonary inflammation, but did not affect constrictor responses of the aortic rings to phenylephrine and K(+) depolarization. In contrast, maximal relaxation of aortic rings to acetylchol...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4030514</comments>
            <pubDate>Tue, 28 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4030514</guid>        </item>
        <item>
            <title>KMUP-1 inhibits pulmonary artery proliferation by targeting serotonin receptors/transporter and NO synthase, inactivating RhoA and suppressingAKT/ERK phosphorylation.</title>
            <link>http://www.medworm.com/index.php?rid=4015790&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20870034%26dopt%3DAbstract</link>
            <description>In conclusion, KMUP-1 inhibits MCT-induced PA proliferation by binding to 5-HT(2A), 5-HT (2B) and 5-HT(2C) receptors, increasing endothelial eNOS/5-HT(2B) receptor expression and NO release, inhibiting 5-HTT/RhoA/ROCK expression and AKT/ERK phosphorylation. KMUP-1 is suggested to be useful in the treatment of 5-HT-induced pulmonary artery proliferation.
    PMID: 20870034 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4015790</comments>
            <pubDate>Wed, 22 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4015790</guid>        </item>
        <item>
            <title>Involvement of asymmetric dimethylarginine and Rho kinase in the vascular remodeling in monocrotaline-induced pulmonary hypertension.</title>
            <link>http://www.medworm.com/index.php?rid=4015792&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20840872%26dopt%3DAbstract</link>
            <description>Authors: Li XH, Peng J, Tan N, Wu WH, Li TT, Shi RZ, Li YJ
    Recent studies have shown that the plasma level of asymmetric dimethylarginine (ADMA) was increased accompanied by the decreased dimethylarginine dimethylaminohydrolase (DDAH) activity in pulmonary hypertension (PH) and ADMA was able to regulate pulmonary endothelial cells mobility through increasing the activity of Rho kinase (ROCK). This work was conducted to explore the role of ADMA/DDAH pathway in vascular remodeling in PH and the underlying mechanisms. The rat model of PH was established by a single injection of monocrotaline (60mg/kg, s.c.). The pulmonary arterial pressure, the remodeling of pulmonary artery, the hypertrophy of right ventricle, the plasma levels of ADMA and NO, the expression of DDAH2, ROCK1 or ROCK2 and ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4015792</comments>
            <pubDate>Wed, 15 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4015792</guid>        </item>
        <item>
            <title>Effects of 17 Î²-estradiol on lipopolysacharride-induced intracellular adhesion molecule-1 mRNA expression and Ca(2+) homeostasis alteration in human endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=4015791&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20843480%26dopt%3DAbstract</link>
            <description>Authors: Thor D, Zhang R, Anderson L, Bose D, DubÃ© GP, Rahimian R
    Recent evidence showed that 17 Î²-estradiol (E(2)) decreased cytokine-induced expression of cell adhesion molecules (CAM). Changes in intracellular Ca(2+) concentration ([Ca(2+)](i)) has been shown to be associated with CAM expression in endothelial cells. Here, the effects of E(2) (1Î¼M, 24h) on the expression of intracellular adhesion molecule-1 (ICAM-1) and [Ca(2+)](i) were investigated in a lipopolysaccharide (LPS) (100ng/mL, 18h)-stimulated human endothelial cell line, EA.hy926, using real-time PCR and spectrofluorometry, respectively. PCR analysis revealed a significant increase in ICAM-1 expression in calcium ionophore A23187 (1nM)- or LPS-stimulated cells. Pretreatment of cells with E(2) significantly inhi...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=4015791</comments>
            <pubDate>Wed, 15 Sep 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">4015791</guid>        </item>
        <item>
            <title>PKG-I Inhibition attenuates vascular endothelial growth factor-stimulated angiogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=3958590&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20813203%26dopt%3DAbstract</link>
            <description>Authors: Koika V, Zhou Z, Vasileiadis I, Roussos C, Finetti F, Monti M, Morbidelli L, Papapetropoulos A
    Vascular endothelial growth factor (VEGF) stimulates nitric oxide (NO) production, which mediates many of its angiogenic actions. However, the angiogenic pathways that operate downstream of NO following VEGF treatment are not well characterized. Herein, we used DT-2 and DT-3, two highly selective cGMP-dependent protein kinase I peptide inhibitors to determine the contribution of PKG-I in VEGF-stimulated angiogenesis. Incubation of chicken chorioallantoic membranes (CAM) with PKG-I peptide inhibitors decreased vascular length in a dose-dependent manner, with DT-3 being more effective than DT-2. Moreover, inhibition of PKG-I with DT-3 abolished the angiogenic response elicited by VEGF ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3958590</comments>
            <pubDate>Sun, 29 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3958590</guid>        </item>
        <item>
            <title>Propranolol suppresses angiogenesis in vitro: Inhibition of proliferation, migration, and differentiation of endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=3903756&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20732454%26dopt%3DAbstract</link>
            <description>Authors: Lamy S, Lachambre MP, Lord-Dufour S, BÃ©liveau R
    Propranolol, a non-selective beta-adrenergic blocking drug, was recently reported to control the growth of hemangiomas, the most common vascular tumor of infancy. However, the mechanisms involved in this effect remain unknown. Here, we demonstrate that propranolol dose-dependently inhibited growth factor-induced proliferation of cultured human umbilical vein endothelial cells (HUVECs) through a G(0)/G(1) phase cell cycle arrest. This was correlated to decreased cyclin D1, cyclin D3, cyclin-dependent kinase CDK6 protein levels, while increases in the CDK inhibitors p15(INK4B), p21(WAF1/Cip1) and p27(Kip1) were observed. Chemotactic motility and differentiation of HUVECs into capillary-like tubular structures in Matrigel were al...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3903756</comments>
            <pubDate>Thu, 19 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3903756</guid>        </item>
        <item>
            <title>Lacidipine has anti-atherosclerotic effects independent of its actions on lipid metabolism and blood pressure.</title>
            <link>http://www.medworm.com/index.php?rid=3874505&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20709189%26dopt%3DAbstract</link>
            <description>Authors: Yetik G, UstÃ¼nes L, Dilsiz OY, Ergul A
    The anti-atherosclerotic effect of lacidipine has been attributed to its actions on cholesterol levels, lipid metabolism or oxidant stress in advanced disease. The purpose of the present experiments was to examine whether lacidipine is protective of intimal thickening and vascular dysfunction in early atherosclerosis in the absence of the hypertension and hypercholesterolemia. A second goal was to determine whether and to what extent MMP-9 and oxidant stress are involved in possible beneficial effects of lacidipine. Lacidipine treatment (5 mg/kg/day, p.o. for 3 weeks) significantly prevented the collar-induced intimal thickening. MMP-9 expressions were increased by collar but not effected by lacidipine treatment. Nitrotyrosine staining...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3874505</comments>
            <pubDate>Wed, 11 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3874505</guid>        </item>
        <item>
            <title>Doxorubicin selectively suppresses mRNA expression and production of endothelin-1 in endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=3874504&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20709190%26dopt%3DAbstract</link>
            <description>Authors: Keltai K, Cervenak L, MakÃ³ V, Doleschall Z, ZsÃ¡ry A, KarÃ¡di I
    Doxorubicin (DXR) is a widely used cytostatic agent, but its administration is limited by its cardiovascular side effects. The endothelium is one of the largest organs in the human body and due to its direct contact with blood; it is exposed to the toxic effects of DXR. The aim of this study was to investigate in endothelial cells the effects of DXR on the expression of genes involved in cardiovascular diseases. We used in vitro cultured human umbilical vein endothelial cells (HUVEC) as a model; gene expression was assessed by SuperArray and qPCR. Out of the 96 representative genes of cardiovascular importance, the expression of only the ET-1 gene changed significantly. ET-1 mRNA expression was 10.9% of the...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3874504</comments>
            <pubDate>Wed, 11 Aug 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3874504</guid>        </item>
        <item>
            <title>Prevention of neointima formation by taurine ingestion after carotid balloon injury.</title>
            <link>http://www.medworm.com/index.php?rid=3813817&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20674770%26dopt%3DAbstract</link>
            <description>We examined the effects of taurine ingestion on intimal thickening following balloon injury. Balloon injury was induced in the left common carotid artery of Wistar rats. Taurine (3% (w/v)) was mixed in the drinking water from 2days prior to, until 14days after the induction of balloon injury. The ratio of intima-to-media was significantly reduced by 26% in the taurine-treated rats at 14days after the induction of injury, which was associated with reduced proliferation of the vascular smooth muscle cells (SMCs) in both the media and the intima. Attenuation of arterial superoxide production by taurine ingestion was evident from the results of both the lucigenin chemiluminescence method and in situ detection by dihydroethidium (DHE) staining. Moreover, LPS-stimulated TNF-alpha production in t...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3813817</comments>
            <pubDate>Wed, 28 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3813817</guid>        </item>
        <item>
            <title>Vascular dilation by Paeonol - a mechanism study.</title>
            <link>http://www.medworm.com/index.php?rid=3781107&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20643226%26dopt%3DAbstract</link>
            <description>In conclusion, our study suggested that voltage-dependent and receptor-operated Ca(2+) channel, as well as intracellular Ca(2+) release were all inhibited by paeonol. An intracellular Ca(2+) regulatory mechanism may be responsible to potent vasodilatory effect of paeonol.
    PMID: 20643226 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3781107</comments>
            <pubDate>Thu, 15 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3781107</guid>        </item>
        <item>
            <title>Pharmacological inhibition of Axl affects smooth muscle cell functions under oxidative stress.</title>
            <link>http://www.medworm.com/index.php?rid=3781106&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20643227%26dopt%3DAbstract</link>
            <description>In conclusion, R428 and R572 are more potent inhibitors of ligand-independent mediated Axl signaling compared to Fc-Axl in RASMs under oxidative stress.
    PMID: 20643227 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3781106</comments>
            <pubDate>Thu, 15 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3781106</guid>        </item>
        <item>
            <title>Poly (ADP-ribose) polymerase-1 [PARP-1] and Its Therapeutic Implications.</title>
            <link>http://www.medworm.com/index.php?rid=3762135&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20633699%26dopt%3DAbstract</link>
            <description>Authors: Sodhi RK, Singh N, Jaggi AS
    Poly (ADP-ribose) polymerases (PARPs) are a family of cell signaling enzymes present in eukaryotes, which are involved in the poly (ADP-ribosylation) of DNA binding proteins. While an 18 member superfamily of PARPs has been identified, however PARP-1 the most abundant isoform accounts for more than 90% of its functions. PARP-1 works as DNA damage nick sensor, which uses NAD(+) to form polymers of ADP ribose (PAR) and nicotinamide. Three consequences of the activation of PARP-1 are particularly important for drug development: first, its role in DNA repair; second, its capacity to deplete cellular energetic pools, which culminates in cell dysfunction and necrosis; and third, its capacity to promote the transcription of pro-inflammatory genes. Conseque...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3762135</comments>
            <pubDate>Sun, 11 Jul 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3762135</guid>        </item>
        <item>
            <title>Molecular mechanism of angiotensin II-induced insulin resistance in aortic vascular smooth muscle cells: Roles of Protein Tyrosine Phosphatase-1B.</title>
            <link>http://www.medworm.com/index.php?rid=3727307&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20601126%26dopt%3DAbstract</link>
            <description>Authors: Ketsawatsomkron P, Stepp DW, Fulton DJ, Marrero MB
    Insulin resistance is an underlying mechanism of type 2 diabetes and its vascular complications. Recent evidence suggests that crosstalk between angiotensin II (Ang II) and the insulin signaling in vascular smooth muscle cell (VSMC) may contribute to cellular insulin resistance. We hypothesized that Ang II inhibits the anti-mitogenic pathways while enhancing the mitogenic pathways stimulated by insulin via activation of Protein Tyrosine Phosphatase-1B (PTP-1B) in VSMC. We found that Ang II significantly inhibited insulin-induced phosphorylation of tyrosine 608 of IRS-1 and serine 473 of Akt, a downstream member of anti-mitogenic pathway of insulin. In contrast, Ang II increased the serine phosphorylation of IRS-1 which was not...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3727307</comments>
            <pubDate>Thu, 24 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3727307</guid>        </item>
        <item>
            <title>Evidence both L-type and non-L-type voltage-dependent calcium channels contribute to cerebral artery vasospasm following loss of NO in the rat.</title>
            <link>http://www.medworm.com/index.php?rid=3727308&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20601125%26dopt%3DAbstract</link>
            <description>Authors: McNeish AJ, Altayo FJ, Garland CJ
    We recently found that block of NO synthase in rat middle cerebral artery caused spasm, associated with depolarizing oscillations in membrane potential (E(m)) that is similar in form but faster in frequency (circa 1Hz) to vasomotion. T-type voltage-gated Ca(2+) channels contribute to cerebral myogenic tone and vasomotion, so we investigated the significance of T-type and other ion channels for membrane potential oscillations underlying arterial spasm. Smooth muscle cell membrane potential (E(m)) and tension were measured simultaneously in rat middle cerebral artery. NO synthase blockade caused temporally coupled depolarizing oscillations in cerebrovascular E(m) with associated vasoconstriction. Both events were accentuated by block of smooth m...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3727308</comments>
            <pubDate>Mon, 21 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3727308</guid>        </item>
        <item>
            <title>Influence of endothelium on beta-adrenoceptor-mediated mechanical and electrical function in rat pulmonary artery.</title>
            <link>http://www.medworm.com/index.php?rid=3696200&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20570752%26dopt%3DAbstract</link>
            <description>Authors: Mahajan P, Tabrizchi R
    The effect of isoprenaline on mechanical and electrical function were studied in intact and denuded rat isolated pulmonary arteries. In intact blood vessels, isoprenaline-induced relaxation was significantly attenuated by acidification of buffer, presence of Ba(2+) and/or ouabain. Isoprenaline produced hyperpolarisation of vascular muscle cells increasing E(m) from -61.0+/-0.44 (n=190 cells) to -70.0+/-0.74mV (n=31 cells; mean+/-SE). The latter effect was inhibited by acidification of buffer, tetraethylammonium (TEA), Ba(2+) and/or ouabain. Isoprenaline-mediated relaxation was also significantly inhibited by the removal of endothelial cells. Acidification of buffer, or presence of Ba(2+), or ouabain alone did not result in further inhibition of relaxatio...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3696200</comments>
            <pubDate>Wed, 02 Jun 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3696200</guid>        </item>
        <item>
            <title>The role of CD40L and VEGF in the modulation of angiogenesis and inflammation.</title>
            <link>http://www.medworm.com/index.php?rid=3677594&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20546942%26dopt%3DAbstract</link>
            <description>Authors: Chakrabarti S, Rizvi M, Morin K, Garg R, Freedman JE
    Recently, there has been growing interest in deciphering the role of angiogenesis in the progression of atherogenesis. Importantly, CD40-CD40L interactions are of significant relevance because of their involvement in both angiogenesis and atherosclerotic development. Previously, we have shown that recombinant soluble CD40 ligand (rsCD40L) stimulates auto-inflammatory CD40L synthesis and reactive oxygen species (ROS) generation in vascular cells. In the current study, we demonstrate that redox-mediated CD40-CD40L interaction can enhance vascular endothelial growth factor (VEGF)-induced angiogenesis, endothelial migration, and actin polymerization processes. Interestingly, addition of exogenous VEGF lead to cleavage of de novo...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3677594</comments>
            <pubDate>Wed, 19 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3677594</guid>        </item>
        <item>
            <title>Paclitaxel chemotherapy and vascular toxicity as assessed by flow-mediated and nitrogen-mediated vasodilatation.</title>
            <link>http://www.medworm.com/index.php?rid=3574123&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20470900%26dopt%3DAbstract</link>
            <description>CONCLUSION: Treatment with paclitaxel-containing combinations impairs endothelial function in vivo but endothelial function deterioration is not related to the serum levels of inflammation markers.
    PMID: 20470900 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3574123</comments>
            <pubDate>Mon, 10 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3574123</guid>        </item>
        <item>
            <title>Activation of Endothelial BK(Ca) Channels Causes Pulmonary Vasodilation.</title>
            <link>http://www.medworm.com/index.php?rid=3574122&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20470901%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: Pulmonary endothelium expresses BK(Ca) channels. Activation of endothelial BK(Ca) channels causes hyperpolarization and NO mediated endothelium-dependent vasodilation in micro- and macrovasculature in the lung.
    PMID: 20470901 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3574122</comments>
            <pubDate>Mon, 10 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3574122</guid>        </item>
        <item>
            <title>Adult rats are more sensitive to the vascular effects induced by hyperhomocysteinemia than young rats.</title>
            <link>http://www.medworm.com/index.php?rid=3550419&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20450986%26dopt%3DAbstract</link>
            <description>Authors: de Andrade CR, de Campos GA, Tirapelli CR, Laurindo FR, Haddad R, Eberlin MN, de Oliveira AM
    We aimed to investigate the vascular effects of hyperhomocysteinemia (HHcy) on carotid arteries from young and adult rats. With this purpose young and adult rats received a solution of DL-homocysteine-thiolactone (1g/kg body weight/day) in the drinking water for 7, 14 and 28days. Increase on plasma homocysteine occurred in young and adult rats treated with DL-homocysteine-thiolactone in all periods. Vascular reactivity experiments using standard muscle bath procedures showed that HHcy enhanced the contractile-response of endothelium-intact, carotid rings to phenylephrine in both young and adult rats. However, in young rats, the increased phenylephrine-induced contraction was observed a...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3550419</comments>
            <pubDate>Mon, 03 May 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3550419</guid>        </item>
        <item>
            <title>Transient signaling of Erk1/2, Akt and PLCgamma induced by nerve growth factor in brain capillary endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=3534514&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20434587%26dopt%3DAbstract</link>
            <description>Authors: Lecht S, Arien-Zakay H, Wagenstein Y, Inoue S, Marcinkiewicz C, Lelkes PI, Lazarovici P
    Cumulative evidences suggest that nerve growth factor (NGF) promotes angiogenic effects such as proliferation and migration of endothelial cells (ECs) from different vascular beds, induces capillary sprouting in chorioallantoic membrane and improves in vivo vascularization in a hind-limb ischemic model. In the present study, we sought to investigate the signaling properties of NGF in a microcapillary ECs model compared to those of a neuronal model. NGF-induced phosphorylation of signaling molecules Erk1/2, Akt and PLCgamma were measured using Western blotting and compared between mouse NGF (mNGF) and snake venom NGF analogues. NGFs-induced signaling was TrkA mediated as evident by inhibitio...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3534514</comments>
            <pubDate>Tue, 27 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3534514</guid>        </item>
        <item>
            <title>4-Aminopyridine-sensitive K(+) channels contributes to NaHS-induced membrane hyperpolarization and relaxation in the rat coronary artery.</title>
            <link>http://www.medworm.com/index.php?rid=3523181&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20430111%26dopt%3DAbstract</link>
            <description>Authors: Cheang WS, Wong WT, Shen B, Lau CW, Tian XY, Tsang SY, Yao X, Chen ZY, Huang Y
    The present study aimed at examining the role of potassium channels and endothelium in relaxations induced by sodium hydrogen sulphide (NaHS), which is the donor of gaseous hydrogen sulphide (H(2)S) and the effect of NaHS on endothelium-dependent relaxations in rat coronary arteries. Rat coronary arteries were suspended in a myograph for force measurement and changes of the membrane potential in arteries were determined by membrane potential-sensitive fluorescence dye. NaHS relaxed coronary arteries pre-contracted by U46619 and the relaxation was significantly less in high KCl-contracted rings. NaHS-induced relaxations were reduced by 4-aminopyridine (4-AP) but unaffected by glibenclamide, iberiotox...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3523181</comments>
            <pubDate>Sun, 25 Apr 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3523181</guid>        </item>
        <item>
            <title>Perinatal changes in superoxide generation in the ovine lung: Alterations associated with increased pulmonary blood flow.</title>
            <link>http://www.medworm.com/index.php?rid=3444111&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20362073%26dopt%3DAbstract</link>
            <description>Authors: Sharma S, Kumar S, Wiseman DA, Kallarackal S, Ponnala S, Elgaish M, Fineman JR, Black SM
    Although alterations in ROS generating systems are well described in several vascular disorders, there is very limited information on the perinatal regulation of these systems in the lung both during normal development and in pulmonary hypertension. Thus, this study was undertaken to explore how the two predominant superoxide generating systems, nicotinamide adenine dinucleotide phosphate-oxidase (NADPH oxidase) and xanthine oxidase (XO), are developmentally regulated in control lambs and in our established lamb model of increased pulmonary blood flow (Shunt) over the first 2months of life. We found that the levels of p47(phox), p67(phox), and Rac1 subunits of NADPH oxidase complex were al...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3444111</comments>
            <pubDate>Mon, 29 Mar 2010 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">3444111</guid>        </item>
        <item>
            <title>Comparable renovascular protective effects of moxonidine and Simvastatin in rats exposed to cigarette smoke.</title>
            <link>http://www.medworm.com/index.php?rid=3429909&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20350618%26dopt%3DAbstract</link>
            <description>This study investigated the effect of the imidazoline I(1)-receptor/alpha(2)-adrenoceptor agonist moxonidine, as compared to the lipid lowering drug simvastatin, on abnormalities induced by cigarette smoke (CS) in renovascular reactivity. Six rat groups were used: control, CS (twice a day for 6weeks), simvastatin, moxonidine, CS+simvastatin, and CS+moxonidine. CS exposure increased plasma urea and creatinine and reduced plasma and renal nitrate/nitrite (NOx). In isolated perfused phenylephrine-preconstricted kidneys of CS rats, vasodilator responses to carbachol or isoprenaline, but not papaverine, were attenuated. Nitric oxide synthase (NOS) inhibition by N(G)-nitro-L-arginine (L-NNA) reduced carbachol vasodilations in control but not CS kidneys, suggesting the impairment of NOS activity ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3429909</comments>
            <pubDate>Fri, 26 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3429909</guid>        </item>
        <item>
            <title>Hemodynamic influences on abdominal aortic aneurysm disease: Application of biomechanics to aneurysm pathophysiology.</title>
            <link>http://www.medworm.com/index.php?rid=3421370&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20347049%26dopt%3DAbstract</link>
            <description>Authors: Dua MM, Dalman RL
    &quot;Atherosclerotic&quot; abdominal aortic aneurysms (AAAs) occur with the greatest frequency in the distal aorta. The unique hemodynamic environment of this area predisposes it to site-specific degenerative changes. In this review, we summarize the differential hemodynamic influences present along the length of the abdominal aorta, and demonstrate how alterations in aortic flow and wall shear stress modify AAA progression in experimental models. Improved understanding of aortic hemodynamic risk profiles provides an opportunity modify patient activity patterns to minimize risk of aneurysmal degeneration.
    PMID: 20347049 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3421370</comments>
            <pubDate>Wed, 24 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3421370</guid>        </item>
        <item>
            <title>Cardiac mast cell proteases do not contribute to the regulation of the rat coronary vascular responsiveness to arterial delivered angiotensin I and II.</title>
            <link>http://www.medworm.com/index.php?rid=3403723&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20307688%26dopt%3DAbstract</link>
            <description>Authors: Bispo-da-Silva LB, Sivieri DO, Prado CM, Becari C, Stuckert-Seixas SR, Pereira HJ, Rossi MA, Oliveira EB, Salgado MC
    Cardiac mast cells (MC) are apposed to capillaries within the heart and release renin and proteases capable of metabolizing angiotensins (Ang). Therefore, we hypothesized that mast cell degranulation could alter the rat coronary vascular responsiveness to the arterial delivered Ang I and Ang II, taking into account carboxypeptidase and chymase-1 activities. Hearts from animals that were either pretreated or not with systemic injection of the secretagogue compound 48/80 were isolated and mounted on a Langendorff apparatus to investigate coronary reactivity. The proteolytic activity of the cardiac perfusate from isolated hearts, pretreated or not with the secretag...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3403723</comments>
            <pubDate>Fri, 19 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3403723</guid>        </item>
        <item>
            <title>Regulation of angiogenesis by a small GTPase Rap1.</title>
            <link>http://www.medworm.com/index.php?rid=3395514&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20302970%26dopt%3DAbstract</link>
            <description>This article provides an overview of these findings in the context of the existing knowledge of the function of the two Rap1 isoforms, followed by speculation regarding potential mechanisms through which Rap1 proteins may be regulating angiogenesis.
    PMID: 20302970 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3395514</comments>
            <pubDate>Tue, 16 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3395514</guid>        </item>
        <item>
            <title>Emodin and rhein inhibit LIGHT-induced monocytes migration by blocking of ROS production.</title>
            <link>http://www.medworm.com/index.php?rid=3387213&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20298810%26dopt%3DAbstract</link>
            <description>In this study, we evaluated the inhibitory effect of emodin and rhein on LIGHT-induced migration in THP-1. Emodin and rhein decreased the level of LIGHT-induced generation of ROS, as well as the expression of CCR1, CCR2 and ICAM-1 and the production of IL-8, MCP-1, TNF-alpha, and IL-6. Emodin and rhein also decreased the phosphorylation of the p38 MAPK and IkB-alpha. Furthermore, the NADPH oxidase assembly inhibitor, AEBSF, and the blocker of NADPH oxidase, p47(phox) small interference RNA (siRNA), also efficiently blocked LIGHT-induced migration, CCR1, CCR2, ICAM-1, and HVEM expression, and p38 MAPK and NF-kB activation. These findings indicate that the inhibitory effects of emodin and rhein on LIGHT-induced migration occur via decreasing ROS production and NADPH oxidase p47(phox) activat...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3387213</comments>
            <pubDate>Mon, 15 Mar 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3387213</guid>        </item>
        <item>
            <title>Effect of high soy diet on the cerebrovasculature and endothelial nitric oxide synthase in the ovariectomized rat.</title>
            <link>http://www.medworm.com/index.php?rid=3338735&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20197113%26dopt%3DAbstract</link>
            <description>Authors: Schreihofer DA, Deutsch C, Lovekamp-Swan T, Sullivan JC, Dorrance AM
    High soy (HS) diets are neuroprotective and promote vascular dilatation in the periphery. We hypothesized that a HS diet would promote vascular dilatation in the cerebrovasculature by mimicking estradiol's actions on the endothelial nitric oxide synthase (eNOS) system including increasing eNOS expression and decreasing caveolin-1 expression to increase nitric oxide (NO) production. Ovariectomized rats were fed HS or a soy-free diet (SF)+/-low physiological estradiol (E2) for 4weeks. Neither E2 nor HS altered middle cerebral artery (MCA) structure or vascular responses to acetylcholine, serotonin, or phenylephrine. Estradiol enhanced bradykinin-induced relaxation in an eNOS-dependent manner. Although E2 and HS...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3338735</comments>
            <pubDate>Sat, 27 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3338735</guid>        </item>
        <item>
            <title>New insights into acute lung injury.</title>
            <link>http://www.medworm.com/index.php?rid=3338736&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20188857%26dopt%3DAbstract</link>
            <description>Authors: Black SM
    
    PMID: 20188857 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3338736</comments>
            <pubDate>Wed, 24 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3338736</guid>        </item>
        <item>
            <title>Endothelial Damage and Stem Cell Repair in Atherosclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=3280590&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20156585%26dopt%3DAbstract</link>
            <description>Authors: Bai X, Wang X, Xu Q
    Atherosclerosis is a slowly progressing and multifactorial disease, in which endothelial dysfunction and damage plays an initial role. Many risk factors for atherosclerosis can lead to endothelial damage of the vessel, especially in the areas where blood flow is disturbed. In the presence of hyperlipidemia, disturbed blood flow results in increased endothelial turnover in the arterial wall. It was demonstrated that disturbed blood flow activates endoplasmic reticulum stress initiating a signal pathway leading to endothelial apoptosis. Following endothelial death, the neighboring mature endothelial cells actively proliferate and migrate to heal the wound. However, stem cell repairing may be needed if endothelial damage is severe. As rapid development of stem...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3280590</comments>
            <pubDate>Fri, 12 Feb 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3280590</guid>        </item>
        <item>
            <title>The lectin-like domain of TNF protects from Listeriolysin-induced hyperpermeability in human pulmonary microvascular endothelial cells - a crucial role for Protein Kinase C-alpha inhibition.</title>
            <link>http://www.medworm.com/index.php?rid=3179536&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20074664%26dopt%3DAbstract</link>
            <description>Authors: Xiong C, Yang G, Kumar S, Aggarwal S, Leustik M, Snead C, Hamacher J, Fischer B, Umapathy NS, Hossain H, Wendel A, Catravas JD, Verin AD, Fulton D, Black SM, Chakraborty T, Lucas R
    Listeriosis can lead to potentially lethal pulmonary complications in newborns and immune compromised patients, characterized by extensive permeability edema. Listeriolysin (LLO), the main virulence factor of Listeria monocytogenes, induces a dose-dependent hyperpermeability in monolayers of human lung microvascular endothelial cells in vitro. The permeability increasing activity of LLO, which is accompanied by an increased reactive oxygen species (ROS) generation, RhoA activation and myosin light chain (MLC) phosphorylation, can be completely inhibited by the protein kinase C (PKC) alpha/beta inhib...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3179536</comments>
            <pubDate>Mon, 11 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3179536</guid>        </item>
        <item>
            <title>Harvesting, identification and barrier function of human lung microvascular endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=3167080&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20060932%26dopt%3DAbstract</link>
            <description>Authors: Catravas JD, Snead C, Dimitropoulou C, Chang AS, Lucas R, Verin AD, Black SM
    Endothelial barrier dysfunction is an important contributor to the pathogenesis of acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Even though approaches that target the prevention and repair of endothelial barrier dysfunction are clearly needed, our understanding of the molecular regulation of pulmonary microvascular endothelial permeability remains incomplete. Cultured pulmonary microvascular endothelial cells represent an attractive paradigm for the study of barrier function. Here, we describe a method for the harvest, identification and culture of human lung microvascular endothelial cells (HLMVEC). HLMVEC thus obtained, grow as a monolayer, exhibit contact inhibition and h...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3167080</comments>
            <pubDate>Thu, 07 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3167080</guid>        </item>
        <item>
            <title>Are newer generation hemoglobin-based oxygen carriers safe: Do they offer an answer?</title>
            <link>http://www.medworm.com/index.php?rid=3167081&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20060496%26dopt%3DAbstract</link>
            <description>Authors: Jahr JS
    
    PMID: 20060496 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3167081</comments>
            <pubDate>Wed, 06 Jan 2010 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3167081</guid>        </item>
        <item>
            <title>Molecular Mechanisms Involved in Adenosine-Induced Endothelial Cell Barrier Enhancement.</title>
            <link>http://www.medworm.com/index.php?rid=3143251&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20045081%26dopt%3DAbstract</link>
            <description>In this study, we demonstrated the adenosine-induced rapid dose-dependent barrier enhancement in human pulmonary artery EC (HPAEC) as measured by an increase in transendothelial electrical resistance (TER). We have shown that HPAEC express only A2A and A2B adenosine receptors. Pharmacological and siRNA depletion studies indicate that A2A, but not A2B receptor activation is required for the adenosine-induced TER increase. Depletion of Galphas with a specific siRNA significantly attenuated the adenosine-induced TER response in HPAEC. In contrast, depletion of either Galphaq or Galphai2 did not affect the adenosine-induced TER increase. This suggests that the adenosine-induced TER increase is cAMP-dependent. The adenosine-induced barrier enhancement effects were associated with a rearrangemen...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3143251</comments>
            <pubDate>Tue, 29 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3143251</guid>        </item>
        <item>
            <title>Alteration in hemodynamic effects of interleukin 2 after treatment with indomethacin in anesthetized rats.</title>
            <link>http://www.medworm.com/index.php?rid=3143250&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20045082%26dopt%3DAbstract</link>
            <description>Authors: Tabrizchi R, Ford CA
    The cardiovascular effects of interleukin 2 (IL2), were investigated in animals pretreated with indomethacin. Bolus intravenous administration of IL2 alone caused a significant reduction in cardiac output over time. Pretreatment with indomethacin significantly accentuated the reduction in cardiac output produced by IL2. The administration of IL2 or indomethacin alone or combined had no significant effects on dP/dt, heart rate or plasma troponin levels. As well, administration of either compound alone or combined had limited effects on mean circulatory filling pressure and arterial blood pressure. Injection of IL2 alone significantly increased resistance to venous return and arterial resistance at 3 hr post injections. Pretreatment with indomethacin caused ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3143250</comments>
            <pubDate>Tue, 29 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3143250</guid>        </item>
        <item>
            <title>High-calcium diet reduces blood pressure, blood volume and preserves vasorelaxation in oral contraceptive-treated female rats.</title>
            <link>http://www.medworm.com/index.php?rid=3126966&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20036339%26dopt%3DAbstract</link>
            <description>Authors: Olatunji LA, Soladoye AO
    Cardiovascular complications are the major clinical challenges among users of synthetic steroids in oral contraceptive (OC) formulations. Interventions that reduce blood volume and improve vasorelaxation have been shown to reduce hypertension and the associated risk factors. The aim of the present study was to investigate the influence of increasing dietary calcium from 0.9 to 3.0% on the development of OC-induced high blood pressure and associated changes in female Sprague-Dawley rats treated with a combination of OC steroids (1mug ethinyl estradiol and 10mug norgestrel; p.o.) daily for 10weeks. Results showed that OC administration led to significant increases in blood pressure, blood volume and cardiac weight. Conversely, OC caused significant reduc...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3126966</comments>
            <pubDate>Wed, 23 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3126966</guid>        </item>
        <item>
            <title>Thyroid hormone: An old drug to new indications.</title>
            <link>http://www.medworm.com/index.php?rid=3123595&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20034595%26dopt%3DAbstract</link>
            <description>Authors: Pantos C, Cokkinos DV
    
    PMID: 20034595 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3123595</comments>
            <pubDate>Mon, 21 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3123595</guid>        </item>
        <item>
            <title>Differential sensitivities of pulmonary and coronary arteries to hemoglobin-based oxygen carriers and nitrovasodilators: Study in a bovine ex-vivo model of vascular strips.</title>
            <link>http://www.medworm.com/index.php?rid=3115844&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20026426%26dopt%3DAbstract</link>
            <description>Authors: Fonseca V, Avizinis J, Moon-Massat P, Freilich D, Kim HW, Hai CM
    Vasoconstriction is a major adverse effect of first and second generation hemoglobin-based oxygen carriers (HBOCs) that hinders their development as blood substitute. However, intravenous infusion of HBOC-201 (second generation) to patients induces significant pulmonary hypertension without significant coronary vasoconstriction. We compared contractile responses of isolated bovine pulmonary and coronary arterial strips to HBOC-201 and HBOC-205LL.LT.MW600 (third generation), polymerized bovine hemoglobins of different molecular weight, and their attenuation by nitroglycerin, sodium nitroprusside (SNP), and sodium nitrite. Pulmonary arteries developed negligible basal tone, but exhibited HBOC-dependent amplificatio...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3115844</comments>
            <pubDate>Fri, 18 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3115844</guid>        </item>
        <item>
            <title>The role of chemokines in recruitment of immune cells to the artery wall and adipose tissue.</title>
            <link>http://www.medworm.com/index.php?rid=3115845&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20026286%26dopt%3DAbstract</link>
            <description>Authors: Surmi BK, Hasty AH
    The role of the immune system is to recognize pathogens, tumor cells or dead cells and to react with a very specific and localized response. By taking advantage of a highly sophisticated system of chemokines and chemokine receptors, leukocytes such as neutrophils, macrophages, and T-lymphocytes are targeted to the precise location of inflammation. While this is a beneficial process for acute infection and inflammation, recruitment of immune cells to sites of chronic inflammation can be detrimental. It is becoming clear that these inflammatory cells play a significant role in the initiation and progression of metabolic disorders such as atherosclerosis and insulin resistance by infiltrating the artery wall and adipose tissue (AT), respectively. Data from huma...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3115845</comments>
            <pubDate>Thu, 17 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3115845</guid>        </item>
        <item>
            <title>Pigment epithelium-derived factor inhibits vascular endothelial growth factor-and interleukin-1beta-induced vascular permeability and angiogenesis in retinal endothelial cells.</title>
            <link>http://www.medworm.com/index.php?rid=3101137&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20006737%26dopt%3DAbstract</link>
            <description>We report that VEGF-and IL-1beta-stimulates permeability, in a dose and time-dependent manner and PEDF inhibits the VEGF-and IL-1beta-induced PREC permeability. In addition, PEDF inhibits the VEGF-and IL-1beta-induced endothelial cell proliferation, migration and tube formation. In addition, overexpression of DN Src blocked both VEGF-and IL-1beta-stimulation of permeability, proliferation and migration, while overexpression of CA Src overpowers the inhibitory action of PEDF on permeability, proliferation and migration. These results demonstrate that PEDF may inhibit the VEGF-and IL-1beta-induced permeability and angiogenesis via Src-dependent pathway.
    PMID: 20006737 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101137</comments>
            <pubDate>Fri, 11 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101137</guid>        </item>
        <item>
            <title>Signaling mechanisms in thyroid hormone-induced cardiac hypertrophy.</title>
            <link>http://www.medworm.com/index.php?rid=3101138&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20005976%26dopt%3DAbstract</link>
            <description>Authors: Ojamaa K
    Cardiac hypertrophy is a significant independent risk factor for increased mortality, comprising of maladaptive changes in cellular, molecular and metabolic processes that ultimately lead to heart failure. However, cardiac hypertrophy represents a continuum from physiological to compensatory to pathological hypertrophy, so that treatment modalities aimed to shift hypertrophy towards the physiological phenotype would represent an attractive therapeutic strategy. Many of the physiological changes caused by thyroid hormone (TH) treatment may provide direct benefit to the failing heart. Recent experimental studies have shown that TH rapidly activates pro-survival PKB/Akt-mTOR signaling pathways, thus providing cytoprotection and increasing synthesis of normal contractile ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101138</comments>
            <pubDate>Thu, 10 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101138</guid>        </item>
        <item>
            <title>Simvastatin activates Akt/glycogen synthase kinase-3beta signal and inhibits caspase-3 activation after experimental subarachnoid hemorrhage.</title>
            <link>http://www.medworm.com/index.php?rid=3101139&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D20004738%26dopt%3DAbstract</link>
            <description>This study was designed to explore the role of simvastatin and its effects on the Akt/GSK3beta survival signal and apoptosis pathway after experimental subarachnoid hemorrhage (SAH). SAH was induced by blood injection into the cisterna magna in New Zealand white rabbits. Increased expression of phospho-Akt and phospho-GSK3beta was observed in brain tissue after SAH. Apoptosis and related proteins, including P53, apoptosis-inducing factor (AIF), cytochrome C, and cleaved caspase-3, were also activated. Simvastatin, at both low dose (10mg/kg) and high dose (40mg/kg), further increased expression of phospho-Akt and phospho-GSK3beta, decreased activation of caspase-3, and inhibited apoptosis. Preserved blood-brain barrier and attenuated brain edema were observed following simvastatin treatment...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3101139</comments>
            <pubDate>Tue, 08 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3101139</guid>        </item>
        <item>
            <title>Mechanisms of nitric oxide synthase uncoupling in endotoxin-induced acute lung injury: Role of asymmetric dimethylarginine.</title>
            <link>http://www.medworm.com/index.php?rid=3067992&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19962451%26dopt%3DAbstract</link>
            <description>In conclusion, this is the first study that suggests a role of the ADMA/DDAH pathway during the development of ALI in mice and that ADMA may be a novel therapeutic biomarker to ascertain the risk for development of ALI.
    PMID: 19962451 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3067992</comments>
            <pubDate>Wed, 02 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3067992</guid>        </item>
        <item>
            <title>Inhibition of endothelial nitric oxide synthase by the lipid phosphatase PTEN.</title>
            <link>http://www.medworm.com/index.php?rid=3067991&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19962452%26dopt%3DAbstract</link>
            <description>Authors: Church JE, Qian J, Kumar S, Black SM, Venema RC, Papapetropoulos A, Fulton DJ
    PTEN (phosphatase and tensin homologue deleted on chromosome 10) is a lipid phosphatase that functions as a negative regulator of the phosphoinositide-3-kinase (PI3K) pathway. The present study sought to examine in depth the interaction between PTEN and eNOS activity. Co-expression of eNOS and PTEN in COS-7 cells significantly decreased NO production compared to eNOS alone, while co-expression of eNOS and the dominant negative mutant PTEN(C124A) significantly increased NO production. Upon examination of the putative eNOS phosphorylation sites, phosphorylation of S116, T497, S617, S635 and S1179 was decreased by PTEN co-expression, while the dominant negative PTEN(C124A) produced an increase in phosph...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3067991</comments>
            <pubDate>Wed, 02 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3067991</guid>        </item>
        <item>
            <title>Human Urotensin II in Internal Mammary and Radial Arteries of Patients Undergoing Coronary Surgery.</title>
            <link>http://www.medworm.com/index.php?rid=3067990&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19962453%26dopt%3DAbstract</link>
            <description>CONCLUSIONS: hU-II is an important spasmogen in arterial grafts with receptors expressed in IMA and RA. hU-II elicits stronger contraction in IMA than in RA and a moderate endothelium-dependent relaxation attributable to nitric oxide, prostacyclin, and endothelium-derived hyperpolarizing factor with involvement of K(Ca) activation. The relaxant response of endothelium-intact IMA and RA to hU-II demonstrates the importance of preservation of endothelium in these grafts.
    PMID: 19962453 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3067990</comments>
            <pubDate>Wed, 02 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3067990</guid>        </item>
        <item>
            <title>Mammalian aminoacyl-tRNA synthetases: Cell signaling functions of the protein translation machinery.</title>
            <link>http://www.medworm.com/index.php?rid=3067989&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19962454%26dopt%3DAbstract</link>
            <description>Authors: Brown MV, Reader JS, Tzima E
    Aminoacyl-tRNA synthetases (aaRSs) are enzymes that join amino acids to tRNAs. Although they are housekeeping enzymes essential for protein synthesis, aaRSs are now known to participate in a wide variety of functions, including transcription, translation, splicing, inflammation, angiogenesis and apoptosis. In eukaryotes, the functional expansion of aaRSs is closely linked to evolutionary advantages conferred by recruitment into protein complexes as well as various structural adaptations. The elucidation and understanding of the diverse functions of aaRSs is a major goal of current and future research. These investigations will undoubtedly provide some of the most fundamental understanding of how and possibly why synthetases became so tightly involv...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3067989</comments>
            <pubDate>Wed, 02 Dec 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3067989</guid>        </item>
        <item>
            <title>Stent based release of a selective PDGF-receptor blocker from the bis-indolylmethanon class inhibits restenosis in the rabbit animal model.</title>
            <link>http://www.medworm.com/index.php?rid=3052812&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19951743%26dopt%3DAbstract</link>
            <description>In conclusion, the application of D-65495 caused a significant decrease in neointima formation, further supporting the concept of using locally released PDGF receptor kinase inhibitors as anti-restenotic agents.
    PMID: 19951743 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3052812</comments>
            <pubDate>Sat, 28 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3052812</guid>        </item>
        <item>
            <title>Vascular activity of a natural diterpene isolated from Croton zambesicus and of a structurally similar synthetic trachylobane.</title>
            <link>http://www.medworm.com/index.php?rid=3052811&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19951744%26dopt%3DAbstract</link>
            <description>In conclusion, these data suggest that vasorelaxant activity of DT is associated with the blockade of L-type voltage-operated calcium channels. Inhibition of NO-dependent relaxation by DT could be related to a decrease in NO availability.
    PMID: 19951744 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3052811</comments>
            <pubDate>Sat, 28 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3052811</guid>        </item>
        <item>
            <title>Circulating smooth muscle progenitor cells in atherosclerosis and plaque rupture: Current perspective and methods of analysis.</title>
            <link>http://www.medworm.com/index.php?rid=3052810&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19951745%26dopt%3DAbstract</link>
            <description>Authors: Bentzon JF, Falk E
    Smooth muscle cells play a critical role in the development of atherosclerosis and its clinical complications. They were long thought to derive entirely from preexisting smooth muscle cells in the arterial wall, but this understanding has been challenged by the claim that circulating bone marrow-derived smooth muscle progenitor cells are an important source of plaque smooth muscle cells in human and experimental atherosclerosis. This theory is today accepted by many cardiovascular researchers and authors of contemporary review articles. Recently, however, we and others have refuted the existence of bone marrow-derived smooth muscle cells in animal models of atherosclerosis and other arterial diseases based on new experiments with high-resolution microscopy a...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3052810</comments>
            <pubDate>Sat, 28 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3052810</guid>        </item>
        <item>
            <title>Thyroid hormone as a therapeutic option for treating ischaemic heart disease: From early reperfusion to late remodelling.</title>
            <link>http://www.medworm.com/index.php?rid=3052809&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19951746%26dopt%3DAbstract</link>
            <description>Authors: Pantos C, Mourouzis I, Cokkinos DV
    Thyroid hormone (TH) , apart from its &quot;classical&quot; actions on cardiac contractility and heart rhythm, appears to regulate various intracellular signaling pathways related to response to stress and cardiac remodelling. There is now accumulating experimental and clinical evidence showing a beneficial effect of TH on limiting myocardial ischaemic injury, preventing / reversing post infarction cardiac remodeling and improving cardiac hemodynamics. Thyroid analogs have already been developed and may allow TH use in clinical practice. However, the efficacy of TH in the treatment of cardiac diseases is now awaited to be tested in large clinical trials.
    PMID: 19951746 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3052809</comments>
            <pubDate>Sat, 28 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3052809</guid>        </item>
        <item>
            <title>Thyroid hormone in cardiac surgery.</title>
            <link>http://www.medworm.com/index.php?rid=3045246&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19945545%26dopt%3DAbstract</link>
            <description>Authors: Ranasinghe AM, Bonser RS
    Thyroid hormone has a wide range of cardiovascular effects which are mediated at both a genomic and non-genomic level. As a stress response to surgery, the non-thyroidal illness syndrome or euthyroid sick syndrome occurs in the post-operative period following cardiac surgery. There remains debate about the potential benefits of the treatment of the non-thyroidal illness syndrome in this setting with acute thyroid hormone supplementation. This review article sets out to discuss the potential benefits of thyroid hormone supplementation and the results from trials relating to both adult and paediatric cardiac surgical population as well as in the setting of brain stem death to optimise the potential cardiac donor.
    PMID: 19945545 [PubMed - as supplied ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=3045246</comments>
            <pubDate>Thu, 26 Nov 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">3045246</guid>        </item>
        <item>
            <title>Vasomotor dysfunction in the thoracic aorta of Marfan syndrome is associated with accumulation of oxidative stress.</title>
            <link>http://www.medworm.com/index.php?rid=2974296&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19879959%26dopt%3DAbstract</link>
            <description>Authors: Yang HH, van Breemen C, Chung AW
    We have described that the progression of thoracic aortic aneurysm in Marfan syndrome is accompanied with aortic vascular dysfunction. In the present study, w hypothesized that the impaired contractile function and endothelial-dependent relaxation could be resulted from oxidative stress in the thoracic aorta. Adrenergic contraction and cholinergic relaxation of thoracic aortae from mice (n=40; age=3, 6, 9months) heterozygous for FBN1 allele (Fbn1C(1039G/+)), a well-defined model of Marfan syndrome, were compared with those from control (n=40). The aortic 8-isoprostane level, an oxidative stress marker, was 32-50% greater in the Marfan group than in the control. Pre-incubation with superoxide dismutase (SOD) improved the phenylephrine-induced co...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2974296</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2974296</guid>        </item>
        <item>
            <title>Thyroid hormone and chronically unloaded hearts.</title>
            <link>http://www.medworm.com/index.php?rid=2974295&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19879960%26dopt%3DAbstract</link>
            <description>Authors: Ito K, Kagaya Y, Shimokawa H
    The heart is subjected to chronic mechanical unloading during prolonged spaceflight and microgravity. The heart in patients with end-stage heart failure is also unloaded in prolonged duration after left ventricular assist devices (LVAD) are implanted. Heterotopic heart transplantation in rats is an established model of chronic cardiac unloading, and has been used to investigate the effects of chronic cardiac unloading on the heart. Observations that have been found using this experimental model are as follow. Chronic cardiac unloading induces time-dependent depressions of Ca(2+) handling and myocyte contractility, which are associated with the shift of myosin heavy chain (MHC) isozymes and altered expressions of Ca(2+) cycling-related proteins. Tre...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2974295</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2974295</guid>        </item>
        <item>
            <title>Thyroid hormone and angiogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=2974294&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19879961%26dopt%3DAbstract</link>
            <description>Authors: Luidens MK, Mousa SA, Davis FB, Lin HY, Davis PJ
    In models of thyroid hormone-induced cardiac hypertrophy, there is appropriate, supportive angiogenesis. Twenty years ago in one such model, angiogenesis in response to the hormone was observed before hypertrophy developed and it is now understood that iodothyronines induce neovascularization in a variety of settings, including the heart, ischemic striated muscle and tumor beds. The molecular mechanism of the pro-angiogenic action of thyroid hormone is both nongenomic and genomic. It is initiated nongenomically at the cell surface receptor for the hormone on integrin alphavbeta3. Kinase transduction of the hormone signal and, ultimately, transcription of several anagiogenesis-relevant genes result. The genes include basic fibrob...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2974294</comments>
            <pubDate>Thu, 29 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2974294</guid>        </item>
        <item>
            <title>Macrophage cholesteryl ester mobilization and atherosclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=2974297&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19878739%26dopt%3DAbstract</link>
            <description>Authors: Ghosh S, Zhao B, Bie J, Song J
    Accumulation of cholesteryl esters (CE) stored as cytoplasmic lipid droplets is the main characteristic of macrophage foam cells that are central to the development of atherosclerotic plaques. Since only unesterified or free cholesterol (FC) can be effluxed from the cells to extracellular cholesterol acceptors, hydrolysis of CE is the obligatory first step in CE mobilization from macrophages. This reaction, catalyzed by neutral cholesteryl ester hydrolase (CEH), is increasingly being recognized as the rate-limiting step in FC efflux. CEH, therefore, regulates the process of reverse cholesterol transport and ultimate elimination of cholesterol from the body. In this review, we summarize the earlier controversies surrounding the identity of CEH in ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2974297</comments>
            <pubDate>Wed, 28 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2974297</guid>        </item>
        <item>
            <title>Thyroid hormone and Myocardial Mitochondrial Biogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=2944732&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19857604%26dopt%3DAbstract</link>
            <description>Authors: Mar&amp;#xED;n-Garc&amp;#xED;a J
    Mitochondria have been central in the development of some of the most important ideas in modern biology. Since the discovery that mitochondria have its own DNA and specific mutations and deletions were found in association with neuromuscular and heart diseases, as well as in aging, an extraordinary number of publications have followed, and the term mitochondrial medicine was coined. Recently, it has been found that thyroid hormone (TH) stimulates cardiac mitochondrial biogenesis increasing myocardial mitochondrial mass, mitochondrial respiration, oxidative phosphorylation (OXPHOS), enzyme activities, mitochondrial protein synthesis (by stimulation in a T3- dependent manner), cytochrome, phospholipid and mtDNA content. Also, TH therapy may modulate card...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2944732</comments>
            <pubDate>Fri, 23 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2944732</guid>        </item>
        <item>
            <title>The cross-talk between Thyroid hormones and the Renin-Angiotensin System.</title>
            <link>http://www.medworm.com/index.php?rid=2944731&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19857605%26dopt%3DAbstract</link>
            <description>Authors: Barreto-Chaves ML, Carrillo-Sep&amp;#xFA;lveda MA, Carneiro-Ramos MS, Gomes DA, Diniz GP
    Thyroid hormones (THs) exert multiple effects on the heart and vascular system. As consequence, altered cardiovascular function observed in the thyroid diseases correspond to one of the most important and clinically relevant aspects found in both hyperthyroidism and hypothyroidism. Beside THs' direct effects on the heart and vascular system, in the last three decades several studies have implicated the Renin-Angiotensin System (RAS) in some of the cardiovascular effects of THs, with this interaction suggesting that RAS may be an important mediator of THs actions. In the present review, we discuss the alterations in the circulating RAS, as well as modifications in cardiac and vascular RAS which...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2944731</comments>
            <pubDate>Fri, 23 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2944731</guid>        </item>
        <item>
            <title>Anti-angiogenic activity of triptolide in anaplastic thyroid carcinoma is mediated by targeting vascular endothelial and tumor cells.</title>
            <link>http://www.medworm.com/index.php?rid=2931484&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19854299%26dopt%3DAbstract</link>
            <description>Authors: Zhu W, He S, Li Y, Qiu P, Shu M, Ou Y, Zhou Y, Leng T, Xie J, Zheng X, Yan G
    Triptolide is confirmed to suppress angiogenesis of anaplastic thyroid carcinoma. Here we further expound the precise mechanism involved in this activity. Triptolide downregulated nuclear factor kappa B (NF-kappaB) pathway and its targeting genes associated with endothelial cells mobilization in human umbilical vein endothelial cells (HUVECs) and impaired VEGF expression in thyroid carcinoma TA-K cells. Furthermore, both triptolide and the conditioned medium from triptolide-treated TA-K cells (CMT) significantly attenuated proliferation, migration and tube formation of HUVECs. In vivo, triptolide inhibited TA-K cells-induced tumor growth, vascular formation and VEGF expression. Our data establish that...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2931484</comments>
            <pubDate>Thu, 22 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2931484</guid>        </item>
        <item>
            <title>Regulation of arteriolar density in adult myocardium during low thyroid conditions.</title>
            <link>http://www.medworm.com/index.php?rid=2925135&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19850151%26dopt%3DAbstract</link>
            <description>Authors: Liu Y, Sherer BA, Redetzke RA, Gerdes AM
    Low thyroid function induced by either propylthiouracil (PTU) treatment or thyroidectomy surgery led to a reduction of arteriolar density in adult rat myocardium, which can be prevented by treatment with thyroxine or the thyroid hormone analogue 3,5-diiodothyropropionic acid (DITPA). However, many questions related to pathophysiological changes and the regulation of arteriolar density in the heart due to hypothyroidism remain unanswered. Sprague Dawley rats were treated with PTU in drinking water for 1, 3, and 6weeks, or co-treated with the vasodilator dipyridamole and PTU for 6weeks, or treated with PTU for 6weeks and treatment discontinued for 2 or 4weeks. Heart mass, body mass, cardiac function and myocardial arteriolar density were ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2925135</comments>
            <pubDate>Mon, 19 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2925135</guid>        </item>
        <item>
            <title>Thyroid hormones and cardiac arrhythmias.</title>
            <link>http://www.medworm.com/index.php?rid=2925134&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19850152%26dopt%3DAbstract</link>
            <description>Authors: Tribulova N, Knezl V, Shainberg A, Seki S, Soukup T
    Thyroid hormone plays an important role in cardiac electrophysiology and Ca(2+) handling through both genomic and nongenomic mechanisms of action, while both actions can interfere. Chronic changes in the amount of circulating thyroid hormone due to thyroid dysfunction or systemic disease result in structural, electrophysiological and Ca(2+) handling remodeling, while acute changes may affect basal activity of cardiac cells membrane systems. Consequently, long-term or rapid modulation of sarcolemmal ion channels, Ca(2+) cycling proteins and intercellular communicating channels by thyroid hormone may affect heart function as well as susceptibility of the heart to arrhythmias. This aspect including pro- and anti-arrhythmic poten...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2925134</comments>
            <pubDate>Mon, 19 Oct 2009 00:00:00 +0100</pubDate>
            <guid isPermaLink="false">2925134</guid>        </item>
        <item>
            <title>Alterations in lung arginine metabolism in lambs with pulmonary hypertension associated with increased pulmonary blood flow.</title>
            <link>http://www.medworm.com/index.php?rid=2891371&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19818875%26dopt%3DAbstract</link>
            <description>This study provides further insights into the molecular mechanisms leading to decreased NO signaling in Shunt lambs and suggests that altered arginine metabolism may play a role in the development of the endothelial dysfunction associated with pulmonary hypertension secondary to increased pulmonary blood flow.
    PMID: 19818875 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2891371</comments>
            <pubDate>Tue, 06 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2891371</guid>        </item>
        <item>
            <title>Androgen deficiency and atherosclerosis: The lipid link.</title>
            <link>http://www.medworm.com/index.php?rid=2891372&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19818414%26dopt%3DAbstract</link>
            <description>Authors: Traish AM, Abdou R, Kypreos KE
    The relationship between androgens deficiency and atherosclerosis is complex, poorly understood, and remains controversial. The aim of this review is to evaluate the data in the literature to determine if androgen deficiency modulates lipid profiles and contributes to atherosclerosis development or progression. Studies in animal and humans suggest that androgen deficiency is associated with increased triglycerides (TG's), total cholesterol (TC), and low-density lipoprotein cholesterol (LDL-C). Although the effects of androgen deficiency on high-density lipoprotein cholesterol (HDL-C) remains controversial, recent data suggest androgen therapy is associated with increased levels of HDL-C and may improve reverse cholesterol transport. Animal studie...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2891372</comments>
            <pubDate>Mon, 05 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2891372</guid>        </item>
        <item>
            <title>Alendronate affects calcium dynamics in cardiomyocytes in vitro.</title>
            <link>http://www.medworm.com/index.php?rid=2880130&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19815094%26dopt%3DAbstract</link>
            <description>Authors: Kemeny-Suss N, Kasneci A, Rivas D, Afilalo J, Komarova SV, Chalifour LE, Duque G
    Therapy with bisphosphonates, including alendronate (ALN), is considered a safe and effective treatment for osteoporosis. However, recent studies have reported an unexpected increase in serious atrial fibrillation (AF) in patients treated with bisphosphonates. The mechanism that explains this side effect remains unknown. Since AF is associated with an altered sarcoendoplasmic reticulum calcium load, we studied how ALN affects cardiomyocyte calcium homeostasis and protein isoprenylation in vitro. Acute and long-term (48h) treatment of atrial and ventricular cardiomyocytes with ALN (10(-8)-10(-6)M) was performed. Changes in calcium dynamics were determined by both fluorescence measurement of cytosol...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2880130</comments>
            <pubDate>Sun, 04 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2880130</guid>        </item>
        <item>
            <title>Thyroid Hormone and Atherosclerosis.</title>
            <link>http://www.medworm.com/index.php?rid=2873064&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19808101%26dopt%3DAbstract</link>
            <description>Authors: Ichiki T
    It is generally accepted that euthyroid state is preferred for the cardiovascular system because both hyperthyroidism and hypothyroidism cause or accelerate cardiovascular diseases. And hypothyroidism is known to be associated with atherosclerosis and ischemic heart diseases. The accelerated atherosclerosis in hypothyroid state has been traditionally ascribed to atherogenic lipid profile, diastolic hypertension and impaired endothelial function. In addition, recent studies suggest that hypothyroidism is associated with the emerging risk factors for atherosclerosis such as hyperhomocysteinemia and an increase in C-reactive protein level. Thyroid hormone also has direct anti-atherosclerotic effects such as blood vessel dilatation, production of vasodilatory molecules, a...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2873064</comments>
            <pubDate>Fri, 02 Oct 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2873064</guid>        </item>
        <item>
            <title>Interaction between bone morphogenetic proteins and endothelin-1 in human pulmonary artery smooth muscle.</title>
            <link>http://www.medworm.com/index.php?rid=2852127&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19786120%26dopt%3DAbstract</link>
            <description>This study examines the regulation of endothelin-1 (ET-1), a potent vasoconstrictor and comitogen that is implicated in the pathogenesis of heritable PAH, by ligands for the BMPR2. Immunohistochemical studies showed that pulmonary artery segments removed from normotensive human lungs express BMPR2 and bone morphogenetic proteins 2, 4 and 7 (BMP2, BMP4 and BMP7). In the presence of BMP7 and BMP4 there was a significant inhibition of ET-1 release, induced by cytokines, from cultured pulmonary artery smooth muscle cells. Fresh ring segments of pulmonary artery were assessed for their response to ET-1 in the presence and absence of BMP2, BMP4 and BMP7. BMP7 inhibited contraction in response to ET-1 in a concentration-dependent manner. BMP2 and BMP4 had no significant effect on the response to ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2852127</comments>
            <pubDate>Thu, 24 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2852127</guid>        </item>
        <item>
            <title>Pharmacological inhibition of the hypertensive response to combretastatin A-4 phosphate in rats.</title>
            <link>http://www.medworm.com/index.php?rid=2783117&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19737629%26dopt%3DAbstract</link>
            <description>In this study, we examined the potential cardiac toxicity and hypertensive effects of CA4P, and defined the most effective pharmacological inhibition of CA4P-induced hypertension in rats. There was a significant, concentration dependent increase in mean arterial blood pressure with a maximum increase of about 60% of the baseline MAP at 30 mg/kg of CA4P compared to the saline control. However, there was no significant increase in the cardiac troponin I level after CA4P injection. Nitroglycerin and the calcium channel blocker diltiazem effectively blocked the hypertensive effects of CA4P while the beta blocker metoprolol was ineffective. Furthermore, sublingual nitroglycerin administration demonstrated an additional anti-hypertensive effect in a setting of a low dose diltiazem infusion (10 m...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2783117</comments>
            <pubDate>Fri, 04 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2783117</guid>        </item>
        <item>
            <title>Diminished Omega-3 Fatty Acids are Associated with Carotid Plaques from Neurologically Symptomatic Patients: Implications for Carotid Interventions.</title>
            <link>http://www.medworm.com/index.php?rid=2778686&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19733689%26dopt%3DAbstract</link>
            <description>Authors: Bazan HA, Lu Y, Thoppil D, Fitzgerald TN, Hong S, Dardik A
    The omega-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), are prevalent in fish oil and their cardioprotective effects are thought to be mediated by anti-inflammatory mechanisms. The aim of this study is to determine whether omega-3 fatty acids are associated with carotid plaques from neurologically symptomatic patients. Plaques were obtained from 41 patients (mean age 62 [44 - 84]; 24-asymptomatic, 17-symptomatic). Intra-plaque lipids were assessed with mass spectrometry. Compared to asymptomatic patients, significantly diminished omega-3 fatty acids DHA (545.8+/-98ng/g vs. 270.7+/-19.6ng/g, p=0.0096) and EPA (385.9+/-68ng/g vs. 216.4+/-17.6ng/g, p=0.0189) were found in carotid plaques from ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2778686</comments>
            <pubDate>Wed, 02 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2778686</guid>        </item>
        <item>
            <title>Withdrawal of fenofibrate treatment partially abrogates preventive neuroprotection in stroke via loss of vascular protection.</title>
            <link>http://www.medworm.com/index.php?rid=2778689&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19732852%26dopt%3DAbstract</link>
            <description>Authors: Ouk T, Laprais M, Bastide M, Gautier S, Mostafa K, Bordet R
    To explore the mechanisms of action of preventive neuroprotection induced by PPAR-alpha activation, we have evaluated the neuronal, vascular effects of preventive treatment with fenofibrate up until the induction of experimental brain ischaemia and fenofibrate treatment withdrawn 3days before ischaemia induction. Fenofibrate (200mg/kg/day) was administered in rats for 14days or withdrawn 3days before induction of cerebral ischaemia. Animals underwent a 1-hour middle cerebral artery occlusion (MCAo), followed by reperfusion for 24h. The MCA's vasoreactivity was analyzed and brain sections were used to assess infarct size, inflammatory and oxidative stress markers. Fenofibrate administration significantly decreases the ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2778689</comments>
            <pubDate>Tue, 01 Sep 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2778689</guid>        </item>
        <item>
            <title>Enhancement of vascular relaxation in rat aorta by phytoestrogens from Curcuma comosa Roxb.</title>
            <link>http://www.medworm.com/index.php?rid=2692732&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19665059%26dopt%3DAbstract</link>
            <description>Authors: Intapad S, Suksamrarn A, Piyachaturawat P
    The present study aims to examine the effects and mechanisms of C. comosa Roxb., an indigenous medicinal plant containing phytoestrogens, on vascular relaxation. Using an organ bath system, acute exposure of intact or endothelium-denuded aortic rings to the hexane extract of C. comosa or an isolated diarylheptanoid compound, D3, did not induce relaxation. However, pre-incubation of aortic rings for 20 mins with hexane extract of C. comosa (10microg/ml) or the isolated diarylheptanoid compound, D3, (0.1, 1 and 10microg/ml) markedly enhanced endothelial-dependent relaxation in response to ACh. The hexane extract did not modulate the relaxation of denuded aortic rings in response to SNP, which suggested a predominant effect on endothelial...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2692732</comments>
            <pubDate>Tue, 04 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2692732</guid>        </item>
        <item>
            <title>Hyperhomocysteinemia Induced by Feeding Rats Diets Rich in DL-Homocysteine Thiolactone Promotes Alterations on Carotid Reactivity Independent of Arterial Structure.</title>
            <link>http://www.medworm.com/index.php?rid=2683602&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19660577%26dopt%3DAbstract</link>
            <description>Authors: de Andrade CR, Tirapelli CR, Haddad R, Eberlin MN, Ramalho LN, Iyomasa MM, Uyemura SA, de Oliveira AM
    We aimed to investigate whether hyperhomocysteinemia (HHcy) interfers on carotid vascular reactivity, and how morphological and functional aspects are related. With this purpose male Wistar rats received a solution of DL-Homocysteine-thiolactone (1g/kg body-weight/day) in the drinking water for 4, 15 and 30days. Lipid profile, carotid artery-morphology and -responsiveness to acetylcholine, phenylephrine and endothelin-1 were analyzed. Similar increase on homocysteine plasmatic levels occurred in rats treated for 4, 15 and 30days. High levels of serum-cholesterol and triglycerides were observed after HHcy 30days. Vascular reactivity experiments using standard muscle bath proced...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2683602</comments>
            <pubDate>Sun, 02 Aug 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2683602</guid>        </item>
        <item>
            <title>Two dissimilar AT(1) agonists distinctively activate AT(1) receptors located on the luminal membrane of coronary endothelium.</title>
            <link>http://www.medworm.com/index.php?rid=2661217&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19643203%26dopt%3DAbstract</link>
            <description>Authors: Castillo-Hern&amp;#xE1;ndez J, Torres-Tirado D, Barajas-Espinosa A, Chi-Ahumada E, Ramiro-D&amp;#xED;az J, Ceballos G, Rubio R
    Diverse intracoronary agonists cause cardiac effects while acting on coronary endothelial luminal membrane (CELM) receptor. Our data show: a) the presence of AT(1)R in isolated CELM and in all cardiac cell types. b) Sustained Intracoronary infusions of: Ang II-POL; a large sized molecule (~15,000kDa) confined to the vessel lumen, that can only act on CELM's AT(1)R or Ang II (~1kDa), both exert the same maximum positive inotropic (PIE) and coronary constriction (CPP). The effects of these two agonists are blocked by Losartan and Sar-POL (~15,000kDa only acts on CELM). Ang II effects are transient due to desensitization and causes tachyphylaxis to Ang II and tow...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2661217</comments>
            <pubDate>Sun, 26 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2661217</guid>        </item>
        <item>
            <title>Resorcylidene aminoguanidine induces antithrombotic action that is not dependent on its anti-glycation activity.</title>
            <link>http://www.medworm.com/index.php?rid=2654773&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19635586%26dopt%3DAbstract</link>
            <description>In conclusion, although RAG and PAG displayed similar anti-glycation and anti-oxidation activities in vitro, only RAG showed antithrombotic activity in vivo that involved activation of COX-2/PGI(2) pathway. Our results indicate that designing novel RAG derivatives with optimal antithrombotic and anti-glycation activities may prove useful to treat diabetic complications.
    PMID: 19635586 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2654773</comments>
            <pubDate>Thu, 23 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2654773</guid>        </item>
        <item>
            <title>Call for a reference model of chronic hind limb ischemia to investigate therapeutic angiogenesis.</title>
            <link>http://www.medworm.com/index.php?rid=2630963&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19619670%26dopt%3DAbstract</link>
            <description>In conclusion, chronic, moderate hind limb ischemia with consistently reduced perfusion levels persisting over a prolonged period can be established reliably in rnu athymic nude rats and is responsive to pro-angiogenic treatments such as EPC transplantation. This study provides a detailed protocol of a highly reproducible reference model to test novel therapeutic options for limb ischemia.
    PMID: 19619670 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2630963</comments>
            <pubDate>Thu, 16 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2630963</guid>        </item>
        <item>
            <title>Anti-angiogenic effect of caffeic acid on retinal neovascularization.</title>
            <link>http://www.medworm.com/index.php?rid=2593338&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19589397%26dopt%3DAbstract</link>
            <description>Authors: Kim JH, Lee BJ, Kim JH, Yu YS, Kim KW
    Pathological angiogenesis is the most common cause of vision loss at all ages including retinopathy of prematurity (ROP), diabetic retinopathy, and age-related macular degeneration. ROP is a proliferative disease of the retinal vasculature in premature infants. Herein, we demonstrated caffeic acid (CA) has the anti-angiogenic activity to retinal endothelial cells and retinal neovascularization in a mouse model of ROP, which might be related to the suppression of ROS-induced VEGF expression. CA effectively inhibited VEGF-induced proliferation of retinal endothelial cells in concentration-dependent manner. In addition, VEGF-induced migration and tube formation of retinal endothelial cells was completely inhibited. This anti-angiogenic activi...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2593338</comments>
            <pubDate>Sun, 05 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2593338</guid>        </item>
        <item>
            <title>Counter-regulation by atorvastatin of gene modulations induced by L-NAME hypertension is associated with vascular protection.</title>
            <link>http://www.medworm.com/index.php?rid=2589036&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19586617%26dopt%3DAbstract</link>
            <description>In conclusion, our data show that atorvastatin specifically antagonizes a set of genes modulated by L-NAME-induced accelerated hypertension.
    PMID: 19586617 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2589036</comments>
            <pubDate>Sat, 04 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2589036</guid>        </item>
        <item>
            <title>Transfection of HGF gene enhances endothelial progenitor cell (EPC) function and improves EPCs transplant efficiency for balloon-induced arterial injury in hypercholesterolemic rats.</title>
            <link>http://www.medworm.com/index.php?rid=2581321&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19577663%26dopt%3DAbstract</link>
            <description>Authors: Song MB, Yu XJ, Zhu GX, Chen JF, Zhao G, Huang L
    Risk factors for coronary heart disease can reduce the number of endothelial progenitor cells (EPC) and impair EPC function, thus hindering their utility in the treatment of cardiovascular diseases. In the present study, we began exploring the feasibility of genetic modification of EPCs with hepatocyte growth factor (HGF) to counter the effects of these risk factors and enhance the biological functions of EPCs. The effects of HGF transfection on proliferation, migration and angiogenesis of EPCs were investigated. Additionally, the role of ERK1/2 in this process was evaluated through the observation of ERK1/2 and ERK1/2 phosphorylation as well as by pharmacological analysis. Finallywe evaluated the effect of HGF-transfected EPCs ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2581321</comments>
            <pubDate>Wed, 01 Jul 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2581321</guid>        </item>
        <item>
            <title>Early inhibition of EGFR signaling prevents diabetes-induced up-regulation of multiple gene pathways in the mesenteric vasculature.</title>
            <link>http://www.medworm.com/index.php?rid=2581323&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19577003%26dopt%3DAbstract</link>
            <description>Authors: Benter I, Benboubetra M, Hollins AJ, Yousif M, Canatan H, Akhtar S
    Diabetes mellitus is associated with vascular complications including an impairment of vascular function and alterations in the reactivity of blood vessels to vasoactive hormones. However, the signaling mechanisms leading to vascular dysfunction in diabetes are not fully understood. This microarray-based study was designed to identify differential gene expression between the normal and diabetic mesenteric vasculature and to investigate the effect of inhibiting epidermal growth factor receptor (EGFR) signaling on global gene expression in the mesenteric bed of streptozocin (STZ)-induced diabetic rats. Transcriptome analysis was performed in triplicate using oligonucleotide microarrays housing 10,000 rat genes on...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2581323</comments>
            <pubDate>Tue, 30 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2581323</guid>        </item>
        <item>
            <title>TW96, a synthetic 1,4-naphthoquinone, differentially regulates vascular and endothelial cells survival.</title>
            <link>http://www.medworm.com/index.php?rid=2581322&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19577004%26dopt%3DAbstract</link>
            <description>In this study, we examined the effects of the novel synthetic naphthoquinone, 2-pyrrilidino-3-(p-hydroxyphenylamino)-1,4-naphthoquinone (TW-96), on cultured VSMCs and endothelial cells (ECs). Pharmacological concentrations of the derivative TW96 were found to induce VSMCs death, probably by increasing ROS levels while decreasing mitochondrial potential DeltaPsi(m)) without affecting ECs. Treatment of tissue cultures with ROS is known to induce MAPK activity. Our observations showed prolonged phosphorylation and perinuclear accumulation of ERK1/2 and p38 simultaneously with an inhibition of MKP1. Increased expression of Bax found in TW96-stimulated VSMCs was inhibited by the NADPH oxidase inhibitor diphenyliodonium (DPI). An examination of the suppressive effects of TW96 on PDGF-BB-stimulat...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2581322</comments>
            <pubDate>Tue, 30 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2581322</guid>        </item>
        <item>
            <title>Specific p38 inhibition in stimulated endothelial cells: A possible new anti-inflammatory strategy after hypothermia and rewarming.</title>
            <link>http://www.medworm.com/index.php?rid=2581324&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19576293%26dopt%3DAbstract</link>
            <description>Authors: Diestel A, Roessler J, Pohl-Schickinger A, Koster A, Drescher C, Berger F, Schmitt KR
    To protect immature organ systems during corrective cardiac surgery, patients are cooled to a minimal temperature of 17 degrees C during cardiopulmonary bypass (CPB). However hypothermic CPB triggers the whole body inflammatory response and results in unwanted prolonged inflammation. The present study was designed to clarify the hypothermia and rewarming induced mechanisms and examine interventional pharmacological strategies that could prevent prolonged inflammation. Stimulated primary human umbilical vein endothelial cells (HUVECs) were exposed to a dynamic temperature protocol analogous to clinical settings. Furthermore endothelial cells were pre-treated with methylprednisolone and/or tacr...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2581324</comments>
            <pubDate>Mon, 29 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2581324</guid>        </item>
        <item>
            <title>Enhanced hypertrophy in ob/ob mice due to an impairment in expression of atrial natriuretic peptide.</title>
            <link>http://www.medworm.com/index.php?rid=2561288&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19560554%26dopt%3DAbstract</link>
            <description>CONCLUSION: This study establishes the role of leptin as an anti-hypertrophic agent during pressure overload hypertrophy, and suggests that a key molecular event is the leptin mediated activation of NFATc4 that regulates the transcriptional activation of the ANP gene promoter.
    PMID: 19560554 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2561288</comments>
            <pubDate>Wed, 24 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2561288</guid>        </item>
        <item>
            <title>Effects of propofol on responses of rat isolated renal arteriole to vasoactive agents.</title>
            <link>http://www.medworm.com/index.php?rid=2532247&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19540932%26dopt%3DAbstract</link>
            <description>Authors: Liu Y, Chang H, Niu L, Xue W, Zhang X, Liang Y, Zhang M
    Rat renal arterial rings were suspended in organ chambers for isometric tension recording. The effects of propofol on the resting tone, KCl-, norepinephrine (NE)-, serotonin- and thromboxane A(2) analog U46619-induced contractions were observed. The relaxation responses to propofol on KCl-, NE- and U46619-induced contractions were assessed in the absence or presence of cyclooxygenase inhibitor, nitric oxide synthetase inhibitor or specific K(+) channel inhibitor. Propofol did not significantly affect the resting tone, but inhibited the contractions induced by KCl-, NE-, serotonin- and U46619. Propofol (1-100 muM) concentration-dependently relaxed 60 mM KCl-, 10 muM NE-, and 1 muM U46619-induced contractions with the value...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2532247</comments>
            <pubDate>Wed, 17 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2532247</guid>        </item>
        <item>
            <title>2-Methoxyestradiol Attenuates Bleomycin-Induced Pulmonary Hypertension and Fibrosis in Estrogen-Deficient Rats.</title>
            <link>http://www.medworm.com/index.php?rid=2532246&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19540933%26dopt%3DAbstract</link>
            <description>This study suggests that 2ME may have protective effects in bleomycin-induced PH and fibrosis. Further investigation of 2ME in pulmonary fibrosis and PH is warranted.
    PMID: 19540933 [PubMed - as supplied by publisher] (Source: Vascular Pharmacology)</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2532246</comments>
            <pubDate>Wed, 17 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2532246</guid>        </item>
        <item>
            <title>PPAR gamma protects cardiomyocytes against oxidative stress and apoptosis via Bcl-2 upregulation.</title>
            <link>http://www.medworm.com/index.php?rid=2532245&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19540934%26dopt%3DAbstract</link>
            <description>Authors: Ren Y, Sun C, Sun Y, Tan H, Wu Y, Cui B, Wu Z
    Cardiovascular disease (CVD) is a leading cause of death and disabilities worldwide. Peroxisome proliferator-activated receptor gamma (PPARgamma) agonists possess potent anti-inflammatory actions and have recently emerged as potential therapeutic agents for CVD. Here we show that H(2)O(2) induced apoptosis in cardiomyocytes with a marked down-regulation of Bcl-2 protein. The PPARgamma agonist rosiglitazone protected cardiomyocytes from oxidative stress and apoptosis. Cardiomyocytes constitutively overexpressing PPARgamma were resistant to oxidative stress-induced apoptosis and protected against impairment of mitochondrial function. On the contrary, cells expressing a dominant negative mutant of PPARgamma were highly sensitive to ox...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2532245</comments>
            <pubDate>Wed, 17 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2532245</guid>        </item>
        <item>
            <title>Reduction of oxidative stress does not attenuate the development of angiotensin II-dependent hypertension in Ren-2 transgenic rats.</title>
            <link>http://www.medworm.com/index.php?rid=2532249&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19539780%26dopt%3DAbstract</link>
            <description>Authors: Kopkan L, Huskov&amp;#xE1; Z, Va&amp;#x148;ourkov&amp;#xE1; Z, Thumov&amp;#xE1; M, Skaroupkov&amp;#xE1; P, Mal&amp;#xFD; J, Kramer HJ, Dvo&amp;#x159;&amp;#xE1;k P, Cervenka L
    Results of our previous studies have suggested that enhanced generation of superoxide (O(2)(-)) may contribute to the pathophysiology of hypertension in Ren-2 transgenic rats (TGR). The present study was performed to evaluate in TGR the effects of chronic treatment with the O(2)(-) scavenger tempol and the antioxidant apocynin on the development of hypertension. Systolic blood pressure (SBP) was monitored from 30 to 99 days of age in TGR and in normotensive Hannover-Sprague Dawley (HanSD) rats. At the end of the experiment, urinary protein and 8-isoprostane excretion were determined and angiotensin II (ANG II) and malondialdehyde (MDA) ...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2532249</comments>
            <pubDate>Mon, 15 Jun 2009 23:00:00 +0100</pubDate>
            <guid isPermaLink="false">2532249</guid>        </item>
        <item>
            <title>NK(1) receptor-mediated endothelium-dependent relaxation and contraction with different sensitivity to post-receptor signaling in pulmonary arteries.</title>
            <link>http://www.medworm.com/index.php?rid=2532248&amp;cid=s_36220_13_f&amp;fid=36220&amp;url=http%3A%2F%2Fwww.ncbi.nlm.nih.gov%2Fentrez%2Fquery.fcgi%3Ftmpl%3DNoSidebarfile%26db%3DPubMed%26cmd%3DRetrieve%26list_uids%3D19539781%26dopt%3DAbstract</link>
            <description>Authors: Miike T, Shirahase H, Kanda M, Kunishiro K, Kurahashi K
    In rabbit intrapulmonary arteries, substance P (SP) has been reported to induce endothelium-dependent relaxation (EDR) and endothelium-dependent contraction (EDC) via tachykinin NK(1) receptors, and endothelium-independent contraction (EIC) via tachykinin NK(2) receptors. The present study pharmacologically examined whether these opposite responses (EDR and EDC) are mediated by the same NK(1) receptor. Five tachykinin agonists, including septide, a reportedly atypical NK(1) agonist, caused concentration-dependent EDR in the presence of NK(2) antagonist (SR-48968)+TXA(2) synthetase inhibitor (ozagrel), which blocked EIC and EDC, in pre-contracted arteries, and concentration-dependent EDC in the presence of NK(2) antagonist...</description>
            <author>Vascular Pharmacology</author>
            <type>journals</type>
        <comments>http://www.medworm.com/rss/comments.php?id=2532248</comments>
            <pubDate>Mon, 15 Jun 2009 23:00:00 +0100</pubDate>
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