Abstract
In vitro and in vivo data provide evidence for an interaction between the renin-angiotensin and fibrinolytic systems. Angiotensin-converting enzyme (ACE) is strategically poised to regulate this interaction. ACE catalyzes the conversion of angiotensin I to angiotensin II (Ang), and Ang II stimulates release of PAI-1, the major inhibitor of tissue-type plasminogen activator (t-PA) and urokinase in the vasculature. Conversely, ACE catalyzes the breakdown of bradykinin, a potent stimulus of t-PA secretion. This interaction between the renin-angiotensin and fibrinolytic systems may partially explain the clinical observation that stimulation or suppression of the renin-angiotensin system can alter the risk of ischemic cardiovascular events. © 1996, Elsevier Science Inc. (Trends Cardiovasc Med 1996;6:239–243).
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