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• W2028685792 abstract "Abstract: Recently, we demonstrated that the endothelium-dependent vasodilator effect of angiotensin(1-7) in the mouse aorta is abolished by genetic deletion of the G protein-coupled receptor encoded by the Mas protooncogene. To circumvent the limitations posed by the possible metabolism of Ang(1-7) in this vessel, in this work we studied the mechanism underlying the vasorelaxant effect of AVE 0991, a nonpeptide mimic of the effects of Ang(1-7), using wild-type and Mas -deficient mice. Ang(1-7) and AVE 0991 induced an equipotent concentration-dependent vasodilator effect in aortic rings from wild-type mice that was dependent on the presence of endothelium. The vasodilator effect of Ang(1-7) and AVE 0991 was completely blocked by 2 specific Ang(1-7) receptor antagonists, A-779 and D-Pro 7 -Ang(1-7), and by inhibition of NO synthase with L-NAME. Moreover, in aortic rings from Mas -deficient mice, the vasodilator effect of both Ang(1-7) and AVE 0991 was abolished. In contrast, the vasodilator effect of acetylcholine and substance P were preserved in Mas -null mice. In addition, the vasoconstriction effect induced by Ang II was slightly increased, and the vasodilation induced by the AT 2 agonist CGP 42112A was not altered in Mas -deficient mice. Our results show that Ang(1-7) and AVE 0991 produced an NO-dependent vasodilator effect in the mouse aorta that is mediated by the G protein-coupled receptor Mas." @default.
• W2028685792 created "2016-06-24" @default.
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• W2028685792 date "2005-09-01" @default.
• W2028685792 modified "2023-10-10" @default.
• W2028685792 title "The Endothelium-Dependent Vasodilator Effect of the Nonpeptide Ang(1-7) Mimic AVE 0991 Is Abolished in the Aorta of Mas-Knockout Mice" @default.
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• W2028685792 doi "https://doi.org/10.1097/01.fjc.0000175237.41573.63" @default.
• W2028685792 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/16116331" @default.
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