Cardiovascular Effects of Aldosterone and Post-Acute Myocardial Infarction Pathophysiology

Jay N. Cohn, Wilson Colucci

Research output: Contribution to journalArticlepeer-review

67 Scopus citations

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.

Original languageEnglish (US)
Pages (from-to)4-12
Number of pages9
JournalAmerican Journal of Cardiology
Volume97
Issue number10 SUPPL. 1
DOIs
StatePublished - May 22 2006

Fingerprint

Dive into the research topics of 'Cardiovascular Effects of Aldosterone and Post-Acute Myocardial Infarction Pathophysiology'. Together they form a unique fingerprint.

Cite this