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Am J Cardiol. 2006 May 22;97(10A):4F-12F. Epub 2006 Apr 5.

Cardiovascular effects of aldosterone and post-acute myocardial infarction pathophysiology.

Author information

  • 1Cardiovascular Division, Department of Medicine, University of Minnesota School of Medicine, Minneapolis, Minnesota 55455, USA. cohnx001@umn.edu

Abstract

Aldosterone is an important mediator of the renin-angiotensin-aldosterone system (RAAS) that plays a major role in the pathophysiology of cardiovascular disease as well as regulation of extracellular fluid volume and potassium. In experimental models, aldosterone has been shown to promote endothelial dysfunction; induce vascular inflammation, myocardial ischemia, and necrosis; increase collagen synthesis in cardiac fibroblasts; contribute to plasminogen activator inhibitor-1 regulation; decrease baroreceptor sensitivity and reflex function; block myocardial uptake of norepinephrine; increase oxidative stress; and stimulate cardiomyocyte apoptosis. A review of animal and human studies with aldosterone blockers reveals improvement in, and in some cases complete reversal of, these pathophysiologic effects of aldosterone on the cardiovascular system.

PMID:
16698330
[PubMed - indexed for MEDLINE]
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