To examine the coronary effects of arginine–vasopressin during reperfusion after a short ischemia, left circumflex coronary artery flow was electromagnetically measured, and 15 min total occlusion of this artery followed by reperfusion was induced in anesthetized goats (five nontreated, five treated with the inhibitor of nitric oxide synthesis Nw-nitro-l-arginine methyl ester (l-NAME) and five treated with the inhibitor of cyclooxygenase meclofenamate). The vasoactive drugs and l-NAME were intracoronarily injected, and meclofenamate by i.v. route. At 60 min of reperfusion, coronary vascular conductance was not changed significantly in nontreated and was decreased by 35% (P<0.01) in l-NAME-treated and by 30% (P<0.01) in meclofenamate-treated animals. During reperfusion, the coronary vasodilatation with acetylcholine (3–100 ng) and sodium nitroprusside (1–10 μg) was not altered in nontreated animals, and the vasodilatation with acetylcholine but not with sodium nitroprusside was partially decreased in l-NAME—but not in meclofenamate-treated animals. The vasoconstriction in response to arginine–vasopressin (0.03–0.3 μg) was increased during reperfusion in nontreated, was not changed in l-NAME-treated and was decreased in meclofenamate-treated animals. Therefore, it is suggested that during reperfusion after a short ischemia: (1) the coronary vasodilator reserve is preserved; (2) the coronary vasodilatation with acetylcholine is also preserved, but in this vasodilatation, the role of nitric oxide may be attenuated and prostanoids may be not involved; and (3) the coronary vasoconstriction with arginine–vasopressin is increased, probably due to both attenuation of the modulatory role of nitric oxide and the release of vasoconstrictor prostanoids.