Cardiovascular Effects of Aldosterone and Post-Acute Myocardial Infarction Pathophysiology

Jay N Cohn, Wilson Colucci

Research output: Contribution to journalArticle

54 Citations (Scopus)

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

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Aldosterone
Myocardial Infarction
Baroreflex
Plasminogen Activator Inhibitor 1
Extracellular Fluid
Renin-Angiotensin System
Cardiovascular System
Cardiac Myocytes
Myocardial Ischemia
Blood Vessels
Norepinephrine
Potassium
Oxidative Stress
Theoretical Models
Necrosis
Cardiovascular Diseases
Collagen
Fibroblasts
Apoptosis
Inflammation

Cite this

Cardiovascular Effects of Aldosterone and Post-Acute Myocardial Infarction Pathophysiology. / Cohn, Jay N; Colucci, Wilson.

In: American Journal of Cardiology, Vol. 97, No. 10 SUPPL. 1, 22.05.2006, p. 4-12.

Research output: Contribution to journalArticle

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