This study was designed to test if nitric oxide (NO) contributes to norepinephrine-induced right coronary vasodilation and if NO blunts the norepinephrine-induced increase in myocardial oxygen consumption (MVO₂) in the right ventricle. In five anesthetized, open chest dogs, mean aortic pressure, heart rate, right ventricular dP/dt, right coronary blood flow, and right ventricular MVO₂ were measured before and during graded intracoronary infusions of norepinephrine in the absence and presence of a NO synthase blocker, N-nitro-L-arginine methyl ester (L-NAME, 150 ug/min, i.c.). During both conditions, right coronary blood flow and right ventricular MVO₂ significantly increased with graded infusions of norepinephrine. L-NAME significantly blunted the coronary hyperemic response to norepinephrine, although L-NAME did not alter the relationship between right ventricular MVO₂ and norepinephrine dose. However, when right ventricular function was indexed by heart rate X right ventricular dP/dt_max X peak right ventricular systolic pressure, L-NAME significantly increased the oxygen cost of right ventricular function. These results indicate that NO contributes to norepinephrine-induced right coronary vasodilation and improves right ventricular oxygen utilization efficiency.