The present study examined the role of nitric oxide in coronary vascular tone and in the coronary vasodilatation in response to β-adrenoceptor stimulation and adenosine. In anesthetized goats, the effects of intracoronary and i.v. administration of the inhibitor of nitric oxide synthesis, N w-nitro- l-arginine methyl ester ( l-NAME), and those of isoproterenol, adenosine and acetylcholine on coronary blood flow, measured electromagnetically in the left circumflex coronary artery, were recorded. Intracoronary infusion of l-NAME (30–40 μg kg −1 min −1, four goats) reduced resting coronary blood flow by 14±3% ( P<0.05) without changing arterial pressure and heart rate. l-NAME (40 mg kg −1, eight goats) i.v. reduced resting coronary blood flow by 19±4% ( P<0.05), increased mean systemic arterial pressure by 22±3% ( P<0.01) and decreased heart rate by 10±2% ( P<0.05). These effects of l-NAME were partially, but significantly reversed by l-arginine (six goats). Isoproterenol (10–100 ng, eight goats), adenosine (0.3–10 μg, seven goats) and acetylcholine (3–100 ng, five goats), injected intracoronarily, increased coronary conductance in a dose-dependent way and, under control conditions, these increases for isoproterenol, ranged from 32±5% to 82±12%; for adenosine, 6±2% to 174±22%; and for acetylcholine, 39±5% to 145±15%. During i.v. l-NAME the increases in coronary conductance induced by isoproterenol and acetylcholine were significantly reduced by about 50 and 60% ( P<0.05), respectively, whereas those induced by adenosine were significantly increased further (about 30–100%, P<0.05). During l-NAME plus l-arginine, the effects of isoproterenol, acetylcholine and adenosine on coronary conductance were not significantly different from those under control conditions. Therefore, it is suggested that in the coronary circulation: (a) nitric oxide may produce a basal vasodilator tone under normal conditions; (b) nitric oxide may be an intermediate in the vasodilatation due to β-adrenoceptor stimulation and acetylcholine, and (c) the vasodilatation due to adenosine is potentiated during reduction of nitric oxide production.