Bradykinin induced dilatation of human epicardial and resistance coronary arteries in vivo: effect of inhibition of nitric oxide synthesis. Issue 5 (1st November 1997)

• Record Type: Journal Article
• Authors: Kato, Masaya; Shiode, Nobuo; Yamagata, Togo; Matsuura, Hideo; Kajiyama, Goro
• Is Part Of: Heart. Volume 78:Issue 5(1997)
• Page Start: 493
• Page End: 498
• Publication Date: 1997-11-01
• Subjects: bradykinin -- nitric oxide -- coronary artery -- coronary blood flow; Heart -- Diseases -- Treatment -- Periodicals; Cardiology -- Periodicals; 616.12
• DOI: 10.1136/hrt.78.5.493
• Languages: English
• ISSNs: 1355-6037

Abstract

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.