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(Hypertension. 2004;43:938.)
© 2004 American Heart Association, Inc.

Editorial Commentaries

The Many Targets of Aldosterone

From the Canadian Institutes of Health Research Multidisciplinary Research Group on Hypertension and Hypertension Clinic, Clinical Research Institute of Montréal, Québec, Canada.

Correspondence to Ernesto L. Schiffrin, MD, PhD, FRCPC, Clinical Research Institute of Montreal, 110 Pine Avenue, West Montreal, Quebec, Canada H2W 1R7. E-mail ernesto.schiffrin@ircm.qc.ca

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

In the current issue of Hypertension, Oberleithner et al¹ demonstrate a new effect of aldosterone acting via mineralocorticoid receptors to stimulate water entry into human endothelial cells. Using atomic force microscopy, these authors show that cultured human umbilical vein endothelial cells respond to aldosterone with sodium and water entry (they swell) and this can be blocked by a mineralocorticoid receptor blocker (spironolactone). Swollen aldosterone-treated endothelial cells shrink when micromolar concentrations of amiloride are applied, concentrations at which amiloride does not inhibit the sodium-proton exchanger. The authors report they already showed that cariporide, a selective inhibitor of the sodium-proton exchanger, does not affect aldosterone-induced endothelial cell swelling.¹ Thus, they suggest that amiloride inhibits a sodium channel similar to the apical epithelial sodium channel in the distal nephron. The authors conclude that sodium channels are induced by genomic effects of aldosterone, which result in sodium influx and cell depolarization, creating an electrochemical gradient that leads to chloride and water accumulation and cell swelling. Amiloride, by blocking the sodium channels, hyperpolarizes the cell, leading to chloride efflux followed by efflux of water and cell shrinkage. Whether this interpretation is correct remains to be proven. The authors propose that endothelial cell swelling followed by sodium influx also leads to activation of the sodium/potassium ATPase and potassium influx. They suggest that, considering the huge surface of endothelium, aldosterone may reduce serum concentrations of potassium not only by its renal action but also mediated by inducing potassium entry into endothelial cells as a result of . . . [Full Text of this Article]

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