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.