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(Hypertension. 2005;46:27.)
© 2005 American Heart Association, Inc.

Editorial Commentaries

Rapid Effects of Aldosterone

Relevant in Cardiac Ischemia?

Martin Wehling

From the Institute of Clinical Pharmacology, University Hospital of Mannheim, Faculty of Clinical Medicine Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer, Mannheim, Germany.

Correspondence to Martin Wehling, Institute of Clinical Pharmacology, University Hospital of Mannheim, Faculty of Clinical Medicine Mannheim, University of Heidelberg, Theodor-Kutzer-Ufer, 68135 Mannheim, Germany. E-mail martin.wehling@kpha.ma.uni-heidelberg.de

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

Not long ago, scientists celebrated the 50th birthday of aldosterone. And yet miracles around this dinosaur steroid hormone are creeping out of the bushes. For a long period, peaceful contentment overwhelmed even critical minds in the light of tremendous successes: the classical way of steroid action through a genomic machinery starting from the well-known intracellular receptors was close to being ideal in explaining both in vitro and in vivo data.

The more recent findings on rapid effects of steroid hormones such as aldosterone including those of Fujita et al¹ in this issue of Hypertension have stirred up our thinking about the mineralocorticoids and virtually all other steroid hormones. They cannot involve only genomic mechanisms because of their hasty appearance and, therefore, have been termed "nongenomic" effects.

Such effects are all but new with the first report for a steroid hormone—progesterone—dating back to the 1940s,² and those for aldosterone dating back to the 1950s and 1960s.^3,4 However, as a consequence of vigorous efforts, the general scientific audience has gradually accepted their existence, and the mechanisms involved are being progressively investigated, at least up to a certain level.

Over the past decade, it has become increasingly clear that those novel steroid actions use very common intracellular signaling pathways that are seemingly promiscuous and, thus, recruited by many other hormones that induce rapid signaling (eg, catecholamines). Though differing from steroid hormone to steroid hormone and from tissue to tissue to a some extent, common themes seem to be involvement of MAP kinases, phospholipase . . . [Full Text of this Article]

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