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.