Role of nitric oxide in coronary arterial vasomotion and the influence of coronary atherosclerosis and its risks

Abstract

Healthy coronary vascular endothelium releases nitric oxide to modulate resting and dynamic coronary arterial tone. We studied the impact of atherosclerosis and/or its risks on endothelial nitric oxide release in response to metabolic stimuli by evaluating coronary vasomotor responses to atrial pacing before and after the inhibition of nitric oxide produciton by intracoronary N G-monomethyl-L-arginine (L-NMMA) (20 μmol/min) infusion. The study includes 34 patients (15 with coronary disease, 11 with normal coronary arteries and ≥1 risk factor, and 8 with normal coronary arteries and no risks). Coronary blood flow was derived from Doppler flow velocity (0.018-inch Doppler wire) and coronary diameter. L-NMMA infusion reduced coronary blood flow by 18 ± 16% and coronary diameter by 10 ± 9%. Responses were identical in all subgroups. Coronary blood flow responses to pacing were similar in all subgroups and were unaffected by L-NMMA (11 ± 11 vs 13 ± 9 ml/min; p = 0.26). Epicardial coronary vasodilation to control pacing occurred in patients with normal coronary arteries with (4.0 ± 5.2%, p = 0.01) or without (8.0 ± 5.2%, p = 0.03) risks, but not in patients with coronary disease (2.8 ± 5.9%). L-NMMA abolished pacing-induced epicardial vasodilation in patients without coronary artery disease, producing a 1.8 ± 5.1% response, which was similar in all subgroups. We conclude that microvascular responses to rapid atrial pacing are not mediated by nitric oxide. Flow-mediated epicardial coronary arterial responses may be nitric oxide dependent.