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We determined whether a 3-minute period of intense cardiac sympathetic stimulation, which is known to release neuropeptide Y (NPY), elicits a sustained poststimulatory coronary vasoconstriction in anesthetized dogs that had received propranolol. We also periodically measured the cardiac chronotropic responses to test vagal stimulations; these responses served as an index of the neuronal release of NPY. In a group of 11 animals, the coronary vascular resistance increased by 14±4% during the sympathetic stimulation. constriction in isolated human coronary arteries.'0 When infused into human coronary arteries in vivo, NPY decreases the coronary blood flow and transiently alters the electrocardiogram." The ability of NPY to constrict coronary vessels has led to the hypothesis that NPY mediates coronary spasm.5 Exogenous NPY was used in all the studies described above. The coronary vascular effects of NPY released from sympathetic nerve endings appear not to have been evaluated in vivo. The present study was therefore designed to determine the physiological role of neurally released NPY on coronary vascular resistance in vivo. The principal aims of our study were to determine whether a 3-minute period of intense cardiac sympathetic stimulation will evoke a sustained coronary vasoconstriction and will potentiate the coronary vascular responses to exogenous NE. Such effects would presumably be mediated by the release of NPY from the sympathetic nerve endings in the coronary vasculature. Materials and Methods PreparationExperiments were conducted on 23 mongrel dogs that weighed between 18 and 27 kg. The animals were

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