BRADYKININ-INDUCED VASODILATION OF HUMAN CORONARY-ARTERIES IN-VIVO - ROLE OF NITRIC-OXIDE AND ANGIOTENSIN-CONVERTING ENZYME

Objectives. The present study aimed to determine the role of nitric ox ide (NO) and angiotensin-converting enzyme (ACE) in bradykinin (BK)-in duced dilation of human coronary arteries in vivo. Background. BK, pro duced by way of the kinin kallikrein system, causes endothelium depend ent vasodilation. However, little is known about the mechanism of BK-i nduced dilation of coronary arteries in humans in vivo. Methods. The e ffects of an inhibitor of NO synthesis and of an ACE inhibitor on BK-i nduced coronary vasodilation were exam ined in 20 patients who had no significant atherosclerotic stenosis in the artery under study. Lumen diameters of the large epicardial coronary arteries and coronary blood flow (CBF) were measured by quantitative coronary arteriography and i ntracoronary Doppler technique. Results. Intracoronary infusion of BK (0.6 and 2.0 mu g/min) increased coronary artery diameter and CBF with no change in arterial pressure or heart rate. The BK induced increase s in coronary artery diameter and CBF were significantly reduced (p < 0.01) after pretreatment with N-G-monomethyl-L-arginine (200 mu mol) a nd were significantly increased (p < 0.01) after pretreatment with ena laprilat (50 mu g). Conclusions. BK-induced dilation of human large ep icardial and resistance coronary arteries is mediated by NO and increa sed by prior ACE inhibition. (C) 1997 hy the American College of Cardi ology.