Angiotensin II-induced vascular endothelial dysfunction through RhoA/Rho kinase/p38 mitogen-activated protein kinase/arginase pathway

Enhanced vascular arginase activity impairs endothelium-dependent vasorelaxation by decreasing l-arginine availability to endothelial nitric oxide (NO) synthase, thereby reducing NO production. Elevated angiotensin II (ANG II) is a key component of endothelial dysfunction in many cardiovascular dise...

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Veröffentlicht in:American Journal of Physiology: Cell Physiology 2011-05, Vol.300 (5), p.C1181-C1192
Hauptverfasser: Shatanawi, Alia, Romero, Maritza J, Iddings, Jennifer A, Chandra, Surabhi, Umapathy, Nagavedi S, Verin, Alexander D, Caldwell, Ruth B, Caldwell, R William
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Sprache:eng
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