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Drug: Estradiol

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Extent of Vascular Remodeling Is Dependent on the Balance Between Estrogen Receptor {alpha} and G-Protein-Coupled Estrogen ReceptorNovelty and Significance Vessels
Estrogens are important regulators of cardiovascular function. Some of estrogen’s cardiovascular effects are mediated by a G-protein–coupled receptor mechanism, namely, G-protein–coupled estrogen receptor (GPER). Estradiol-mediated regulation of vascular cell programmed cell death reflects the balance of the opposing actions of GPER versus estrogen receptor α (ERα). However, the significance of these opposing actions on the regulation of vascular smooth muscle cell proliferation or migration in vitro is unclear, and the significance in vivo is unknown. To determine the effects of GPER activation in vitro, we studie...
Source: Hypertension - October 11, 2016 Category: Cardiology Authors: Gros, R., Hussain, Y., Chorazyczewski, J., Pickering, J. G., Ding, Q., Feldman, R. D. Tags: Cell Signaling/Signal Transduction, Smooth Muscle Proliferation and Differentiation, Vascular Biology, Vascular Disease Original Articles Source Type: research

Testosterone Alters Maternal Vascular Adaptations: Role of the Endothelial NO System Pregnancy
In conclusion, increased maternal T, at concentrations relevant to abnormal clinical conditions, cause hypertension associated with blunting of NO-mediated vasodilation. T may induce the increased vascular resistance associated with pregnancy-induced hypertension.
Source: Hypertension - February 13, 2013 Category: Cardiology Authors: Chinnathambi, V., Balakrishnan, M., Ramadoss, J., Yallampalli, C., Sathishkumar, K. Tags: Other hypertension, Endothelium/vascular type/nitric oxide Pregnancy Source Type: research

Activation of PI3K/Akt pathway mediated by estrogen receptors accounts for estrone-induced vascular activation of cGMP signaling.
This study investigated the role of estrogen receptors and endothelial signaling pathways in the vascular relaxation promoted by E1. Aortic rings from male Wistar rats (250-300 g) were contracted with phenylephrine and stimulated with graded concentrations of E1. The concentration-dependent relaxation induced by E1 was abolished after removal of the endothelium or incubation with the estrogen receptor antagonist ICI 182,780. G protein-coupled estrogen receptor antagonism did not alter the E1 effect. Pretreatment of endothelium-intact arteries with inhibitors of nitric oxide synthase, guanylyl cyclase, calmodulin (CaM) an...
Source: Vascular Pharmacology - July 31, 2018 Category: Drugs & Pharmacology Authors: de Oliveira TS, de Oliveira LM, de Oliveira LP, da Costa RM, de Cassia Tostes R, de Castro Georg R, Costa EA, de Souza Lobato N, Filgueira FP, Ghedini PC Tags: Vascul Pharmacol Source Type: research

Renal Vascular Response to Angiotensin II Administration in Two Kidneys-One Clip Hypertensive Rats Treated with High Dose of Estradiol: The Role of Mas Receptor
CONCLUSION: Hypertension induced by 2K1C may attenuate the role of A779 and estradiol in renal vascular responses to Ang II infusion. Perhaps, this response can be explained by the reduction of Ang II type 1 receptor (AT1R) expression in the 2K1C hypertensive rats.PMID:33747565 | PMC:PMC7943267 | DOI:10.1155/2021/6643485
Source: International Journal of Vascular Medicine - March 22, 2021 Category: Cardiology Authors: Samira Choopani Mehdi Nematbakhsh Source Type: research