Bradykinin induced dilatation of human epicardial and resistance coronary arteries in vivo: Effect of inhibition of nitric oxide synthesis

Abstract

Objective - To clarify whether endothelium derived nitric oxide contributes to exogenous bradykinin induced dilatation of human epicardial and resistance coronary arteries in vivo. Design - Quantitative coronary angiography and Doppler flow velocity measurements were used to determine the effects of the nitric oxide synthesis inhibitor, N(G)-monomethyl-L-arginine (L-NMMA), on bradykinin induced dilatation of the epicardial and resistance coronary arteries. Setting - Hiroshima University Hospital. Patients - 20 patients (16 men and four women, mean (SD) age 56 (9) years) with angiographically normal smooth epicardial coronary arteries. Interventions - Serial infusions of bradykinin (0.5, 1.5, and 2.5 μg/min) were given into the left coronary ostium before and after L-NMMA infusion (60 μmol/min). Main outcome measures -Epicardial coronary diameter, coronary blood flow, and coronary vascular resistance. Results - Bradykinin-induced epicardial coronary vasodilatation after L-NMMA (dilatation by 2.5 μg/min, 3.8(1.4)% in the proximal and 5.9(1.8)% in the distal segments, mean (SEM)) was less (p < 0.001, respectively) than before L-NMMA (11.7(2.5)% and 15.1(2.0)%, respectively). In contrast, L-NMMA did not affect the bradykinin induced increase in coronary blood flow and decrease in coronary vascular resistance. Conclusions - Endothelium derived nitric oxide contributes to bradykinin induced dilatation of epicardial coronary arteries, but may be less important in coronary resistance vasodilatation.