The purpose of the present study was to determine whether sympathetic coronary vasoconstrictor responses are altered after brief ischemia and reperfusion. Adult mongrel dogs were anesthetized and instrumented for measurements of heart rate, arterial pressure, left ventricular pressure, left ventricular dP/dt, anterior myocardial wall thickening, and left circumflex coronary artery (LCX) and left anterior descending coronary artery (LAD) blood flow velocities. Changes in coronary vascular resistance were recorded during intravenous bolus doses of norepinephrine and bilateral electrical stimulation of the stellate ganglia. After β-adrenergic blockade and bilateral vagotomy, electrical stimulation of the stellate ganglia increased coronary vascular resistance in the LAD and LCX beds by 38±5% and 39±5%, respectively. After a 15-minute LAD occlusion, repeat electrical stimulation produced increases in coronary resistance of 16±3% and 45±8%, respectively (p<0.05 for the LAD before versus after the occlusion). The peak increase in coronary vascular resistance to two doses of norepinephrine was unchanged. After a shorter period of myocardial ischemia (7 minutes), similar increases in coronary resistance to stellate stimulation were observed before (27±4%) and after (26±6%) myocardial ischemia. The mechanism of this impaired sympathetic coronary vasoconstriction was further tested by examining the responses to bretylium and tyramine. Brief ischemia did not alter the coronary constrictor responses to either bretylium or tyramine, suggesting that mechanisms governing prejunctional release of norepinephrine are intact in the postischemic coronary arterial bed. The postischemic myocardium was characterized by mild reductions in left ventricular dP/dt and marked reductions in transmural myocardial wall thickening, characteristic of myocardial stunning. We conclude that after brief myocardial ischemia, coronary vasoconstriction to sympathetic activation is impaired, whereas constriction to direct receptor activation (norepinephrine) and stimulated prejunctional release of a neurotransmitter (bretylium or tyramine) remain intact. These data are consistent with the interpretation that sympathetic efferent neural conduction is impaired in regions of stunned myocardium.