Thrombotic effects of angiotensin

D. E. Vaughan*

*Corresponding author for this work

Research output: Contribution to journalShort surveypeer-review

2 Scopus citations

Abstract

Reduced risk of myocardial infarction (MI) mortality with angiotensin-converting enzyme (ACE) inhibition suggests a link between the renin-angiotensin-system (RAS) and fibrinolytic function. Excessive endothelial production of plasminogen activator inhibitor type 1 (PAI-1) and deficient endothelial secretion of tissue-type plasminogen activator (t-PA) are associated with thrombosis and ischemic events, such as stroke, atherosclerosis, and MI. Angiotensin II (A-II) regulates PAI-1 production. Suppression of A-II formation by ACE inhibitors likely has a positive effect on Fibrinolytic balance by reducing the production of PAI-1. ACE inhibition also enhances bradykinin levels, which, in turn, increases t-PA secretion and further reduces thrombotic tendency.

Original languageEnglish (US)
Pages (from-to)44-49
Number of pages6
JournalJournal of Myocardial Ischemia
Volume7
Issue numberSUPPL. 1
StatePublished - Jan 1 1995

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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