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Hypertension. 2007;49:728-739
Published online before print February 19, 2007, doi: 10.1161/01.HYP.0000259797.48382.b2
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(Hypertension. 2007;49:728.)
© 2007 American Heart Association, Inc.


Brief Reviews

Nongenomic Actions of Aldosterone on the Renal Tubule

David W. Good

From the Departments of Medicine and Neuroscience and Cell Biology, University of Texas Medical Branch, Galveston.

Correspondence to David W. Good, 4.200 John Sealy Annex, University of Texas Medical Branch, 301 University Blvd, Galveston, TX 77555-0562. E-mail dgood@utmb.edu


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


*    Introduction
 
Aldosterone plays a major role in the maintenance of sodium, potassium, and acid-base balance through its effects on renal electrolyte excretion. This regulation is achieved through aldosterone-induced stimulation of Na+ absorption, K+ secretion, and H+ secretion by the distal nephron, particularly segments of the collecting duct.1–3 These classical actions are mediated through binding of aldosterone to the intracellular mineralocorticoid receptor (MR). The hormone-receptor complex translocates to the nucleus, where it promotes gene transcription and the production of proteins that modulate the expression and activity of the epithelial Na+ channel (ENaC) and other ion transport proteins.1,4–6 Regulatory actions of aldosterone via the MR play an important role in the normal maintenance of blood pressure but also have been implicated in the pathogenesis of hypertension and the progression of renal disease.6–9

In addition to their classical actions, aldosterone and other steroid hormones influence cell processes through nongenomic mechanisms.10,11 Nongenomic effects of aldosterone have been demonstrated in many different epithelial and nonepithelial tissues and are defined by (1) an insensitivity to inhibitors of transcription (actinomycin D) and translation (cycloheximide) and (2) a rapid time course (seconds to a few minutes) that is incompatible with gene regulation and de novo protein synthesis. A rapid onset of action is a sufficient but not necessary criterion for a nongenomic effect. Some nongenomic effects can occur with a slower time course. An additional feature often associated with nongenomic effects is that they are not blocked by spironolactone and/or other MR antagonists, consistent with mediation via a nonclassical . . . [Full Text of this Article]




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