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Hypertension. 2006;47:636-637
Published online before print March 6, 2006, doi: 10.1161/01.HYP.0000205225.88721.2c
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(Hypertension. 2006;47:636.)
© 2006 American Heart Association, Inc.


Editorial Commentaries

Nongenomic Renal Effects of Aldosterone

Dependency on NO and Genomic Actions

Tae-Yon Chun; J. Howard Pratt

From the Department of Medicine, Indiana University School of Medicine and the Richard L. Roudebush V.A. Medical Center, Indianapolis, In.

Correspondence to J. Howard Pratt, MD, R.L. Roudebush VA Medical Center, 1481 W 10th St, Indianapolis, IN 46202. E-mail johpratt@iupui.edu


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

There is increasing evidence for a dependency on aldosterone in the development of hypertension.1 How aldosterone influences the physiology that determines blood pressure or for that matter promotes the pathophysiology of high blood pressure turns out to be less than straightforward. There is the genomic pathway that begins with the binding of aldosterone to the classical mineralocorticoid receptor (MR) and ends with sodium reabsorption at the distal nephron. But aldosterone can convey nongenomic influences as well, actions that have received less attention, possibly in part because they seem counterintuitive to our genomic view of biology. Adding to the complexity of aldosterone’s actions is the fact that there are also nonepithelial (nondistal nephron) targets of aldosterone, such as the heart, the vasculature, the kidney, and other sites. In this issue of Hypertension, Schmidt et al2 describe a rapid (thus nongenomic) effect of administered aldosterone to increase resistance in renal vasculature (a nonepithelial target) in healthy human subjects. The findings follow on the heels of a rather large body of work on the genomic actions of aldosterone.

Aldosterone’s nongenomic effects were first recognized more than a decade before an aldosterone-inducible gene was identified in the late 1990s.3 A nongenomic action characteristically occurs almost immediately, usually within several minutes,4 before sufficient time has elapsed for gene transcription and synthesis of new protein (the time it takes aldosterone to increase the sodium current, a genomic effect, is {approx}30 minutes). A novel aldosterone receptor for nongenomic signaling has yet to be identified, but it . . . [Full Text of this Article]


Related Article:

Rapid Nongenomic Effects of Aldosterone on the Renal Vasculature in Humans
Bernhard M.W. Schmidt, Ulla Sammer, Ingrid Fleischmann, Markus Schlaich, Christian Delles, and Roland E. Schmieder
Hypertension 2006 47: 650-655. [Abstract] [Full Text] [PDF]



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