EFFECTS OF N-NITRO-L-ARGININE ON CORONARY-ARTERY TONE AND REACTIVE HYPEREMIA AFTER BRIEF CORONARY-OCCLUSION IN CONSCIOUS DOGS

Aim: To determine the role of an endothelium-derived relaxing factor ( nitric oxide) in controlling basal coronary tone and coronary vasomoti on after brief coronary occlusion (reactive hyperemia). Methods: In 10 chronically instrumented conscious dogs, we studied the diameter chan ges of the large epicardial coronary artery and coronary blood flow in response to intracoronary administration of acetylcholine (0.1 and 1 mu g) and brief coronary occlusion for 5 and 20 s before and after int racoronary infusion of N-nitro-L-arginine (LNNA). Results: Intracorona ry infusion of LNNA (1, 3, and 10 mg) decreased the diameter of the la rge epicardial coronary artery and coronary blood flow in a dose-depen dent manner without altering arterial pressure and heart rate. LNNA (1 0 mg) significantly attenuated the increase in artery diameter and cor onary blood flow by acetylcholine. The ratio of artery dilation to the blood flow response after acetylcholine was not affected by LNNA. LNN A (10 mg) significantly decreased the ratio of repayment to debt flow volume of reactive hyperemia, but did not affect the ratio of peak to resting flow; if also significantly attenuated the reactive dilation o f the large epicardial coronary artery after reactive hyperemia. The r atio of artery dilation to repayment flow volume (mu m/ml) during reac tive hyperemia was attenuated significantly by LNNA. Conclusion: These findings suggest that endothelium-derived nitric oxide may contribute to basal coronary tone and that reactive dilation of the large epicar dial coronary artery during reactive hyperemia was caused by flow-medi ated nitric oxide release, whereas coronary artery dilation after acet ylcholine was caused largely by the direct receptor-mediated release o f nitric oxide.