The renin-angiotensin system and fibrinolysis

Douglas E. Vaughan*

*Corresponding author for this work

Research output: Contribution to journalArticle

75 Scopus citations

Abstract

In addition to causing vasoconstriction and the retention of salt and water, angiotensin inhibits fibrinolysis, thereby promoting clot formation and protecting against hemorrhage. Activation of the renin-angiotensin system (RAS) can disturb the balance of the fibrinolytic system by stimulating excess production of plasminogen activator inhibitor type 1 (PAI-1) and increasing the risk of thrombotic events. This risk is exacerbated by angiotensin-converting enzyme (ACE)-induced degradation of bradykinin, which normally stimulates production of tissue-type plasminogen activator (t-PA). Modification of the RAS via ACE inhibition may protect against thrombosis by limiting vascular expression of PAI-1 and augmenting bradykinin-induced production of t-PA. Survivors of myocardial infarction treated with an ACE inhibitor have demonstrated a reduction in PAI-1 activity and preservation of the normal ratio of PAI-1 to t-PA. This effect on the fibrinolytic system may contribute to the favorable impact ACE inhibition has been demonstrated to have on the incidence of recurrent myocardial infarction.

Original languageEnglish (US)
Pages (from-to)12-16
Number of pages5
JournalAmerican Journal of Cardiology
Volume79
Issue number5 A
DOIs
StatePublished - Mar 6 1997

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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