Cardiovascular effects of aldosterone and post-acute myocardial infarction pathophysiology.
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.
Cohn
Jay N
JN
Cardiovascular Division, Department of Medicine, University of Minnesota School of Medicine, Minneapolis, Minnesota 55455, USA. cohnx001@umn.edu
Colucci
Wilson
W
D000450:Aldosterone / Q000502:physiology*; D000818:Animals; D006801:Humans; D000451:Mineralocorticoid Receptor Antagonists / Q000627:therapeutic use; D009203:Myocardial Infarction / Q000188:drug therapy / Q000503:physiopathology*; D020257:Ventricular Remodeling / Q000187:drug effects / Q000502:physiology*
D000451:Mineralocorticoid Receptor Antagonists; D000450:Aldosterone