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(Hypertension. 2004;43:e30.)
© 2004 American Heart Association, Inc.

Letters to the Editor

Rapid Nongenomic Effect of Aldosterone on Vasoconstriction

Physiology and Pharmacology, University of Southern Denmark, Odense, Denmark

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

Schmidt et al¹ recently reported in Hypertension that aldosterone has a rapid nongenomic vasodilatory effect when infused into the human forearm. Schmitt et al² published a counterpoint to this report by referring to two studies showing the opposite.

While we have no intention to interfere in the discussion on the complexity of human forearm studies, we wish to call the attention to two independent animal studies published recently in Hypertension’s sister journals Circulation³ and Circulation Research.⁴ Using in vitro techniques (rat aortic rings and rabbit renal afferent arterioles) it was shown that aldosterone decreases vascular reactivity to phenylephrine and to depolarization. This novel effect was seen already at subpicomolar concentrations of aldosterone, and it was mediated by the mineralocorticoid receptor. Furthermore, the effect of aldosterone was seen within 5 minutes and was not blocked by inhibition of gene transcription, allowing the conclusion that the effect is nongenomic. As to the effector mechanism, both studies concluded that the effect of aldosterone involved phosphatidylinositol 3-kinase-dependent nitric oxide synthase activation and production of nitric oxide. Although these two studies did not report any effect of aldosterone on basal tone of the vessels, Arima et al⁵ recently observed that aldosterone increased basal tone in microperfused afferent arterioles by a mechanism dependent on phospholipase C and calcium mobilization in the smooth muscle cells.

Taken together, the studies support the contention of Schmidt et al¹ that the effects of aldosterone on vascular function are complex and are likely to depend on . . . [Full Text of this Article]

Bernhard M.W. Schmidt; Roland E. Schmieder

Department of Medicine IV/Nephrology, University of Erlangen-Nürnberg, Germany