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Circulation. 2003 Nov 11;108(19):2400-6. Epub 2003 Oct 13.

Aldosterone regulates vascular reactivity: short-term effects mediated by phosphatidylinositol 3-kinase-dependent nitric oxide synthase activation.

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  • 1Department of Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada.



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.


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.


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.

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