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• W2015973293 abstract "Very little is known regarding the mechanisms of action of angiotensin II (Ang II) or the consequences of Ang II-dependent hypertension in the cerebral circulation. We tested the hypothesis that Ang II produces constriction of cerebral arteries that is mediated by activation of AT 1A receptors and Rho-kinase. Basilar arteries (baseline diameter ~130 µm) from mice were isolated, cannulated and pressurized to measure the vessel diameter. Angiotensin II was a potent constrictor in arteries from male, but not female, mice. Vasoconstriction in response to Ang II was prevented by an inhibitor of Rho-kinase (Y-27632) in control mice, and was reduced by ~85% in mice deficient in expression of AT 1A receptors. We also examined the chronic effects of Ang II using a model of Ang II-dependent hypertension, mice which overexpress human renin (R + ) and angiotensinogen (A + ). Responses to the endothelium-dependent agonist acetylcholine were markedly impaired in R + A + mice (P < 0.01) compared with controls, but were restored to normal by a superoxide scavenger (PEG-SOD). A-23187 (another endothelium-dependent agonist) produced vasodilation in control mice, but no response or vasoconstriction in R + A + mice. In contrast, dilation of the basilar artery in response to a NO donor (NONOate) was similar in R + A + mice and controls. Thus, Ang II produces potent constriction of cerebral arteries via activation of AT 1A receptors and Rho-kinase. There are marked gender differences in cerebral vascular responses to Ang II. Endothelial function is greatly impaired in a genetic model of Ang II-dependent hypertension via a mechanism that involves superoxide." @default.
• W2015973293 created "2016-06-24" @default.
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• W2015973293 date "2005-08-10" @default.
• W2015973293 modified "2023-10-15" @default.
• W2015973293 title "Cerebral Vascular Effects of Angiotensin II: New Insights from Genetic Models" @default.
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• W2015973293 doi "https://doi.org/10.1038/sj.jcbfm.9600204" @default.
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