Aldosterone Regulates Vascular Reactivity
Short-Term Effects Mediated by Phosphatidylinositol 3-Kinase–Dependent Nitric Oxide Synthase Activation
This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.
Background— There is increasing evidence for rapid nongenomic effects of aldosterone. Therefore, we studied the immediate effects of aldosterone on vascular reactivity in rat aortic ring segments and on endothelial and vascular smooth muscle cellular responses.
Methods and Results— In endothelium-intact ring segments, aldosterone attenuated phenylephrine-mediated constriction (maximal reduction, 25±4% below control phenylephrine-mediated constriction). In contrast, in endothelium-denuded vessels, aldosterone mediated a monophasic dose-dependent enhancement of vasoconstrictor response. In endothelial cells, aldosterone caused a phosphatidylinositol 3-kinase (PI3K)–dependent increase in nitric oxide synthase activity as well as PI3K-dependent activation of extracellular signal–regulated kinase 1/2 and p70 S6 kinase.
Conclusions— Overall, these data support a novel effect of aldosterone on vascular endothelial and smooth muscle cell function. These rapid effects of aldosterone might be important in both the short- and long-term regulation of peripheral vascular resistance. Furthermore, in the setting of endothelial dysfunction, alterations in aldosterone’s short-term vascular responses might contribute to its pathophysiological effects in cardiovascular disease.
Received September 30, 2002; de novo received March 31, 2003; revision received July 9, 2003; accepted July 10, 2003.