Intense sympathetic stimulation releases neuropeptide Y but fails to evoke sustained coronary vasoconstriction in dogs.

Abstract

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. After cessation of stimulation, however, coronary vascular resistance returned rapidly to its control value. The cardiac responses to the test vagal stimuli were attenuated by approximately 40% after cessation of sympathetic stimulation, and this inhibitory effect persisted for approximately 60 minutes. In a second group of eight dogs, we determined whether the intense sympathetic stimulation potentiates the coronary vascular responses to exogenous norepinephrine (NE). Before sympathetic stimulation, standard intracoronary infusions of NE increased coronary vascular resistance by 14 +/- 2%. Intense antecedent sympathetic stimulation did not alter the coronary vascular responses to subsequent NE infusions. However, the chronotropic responses to test vagal stimuli were initially attenuated by approximately 30%, and this inhibitory effect persisted for approximately 1 hour. In a third group of four dogs, we found that exogenous NPY significantly potentiated the coronary vasoconstriction evoked by NE infusions. The coronary vascular responses to combined infusions of NE and NPY were consistently greater (by approximately 13%) than the sum of the responses to these substances when they were infused separately. We conclude that, even though sufficient NPY appears to be released from the sympathetic nerve endings to inhibit vagal neurotransmission, the quantity of NPY released into the coronary blood vessels under the conditions of our experiments appears to be insufficient either to elicit a sustained coronary vasoconstriction or to potentiate the vasoconstrictor effects of intracoronary NE infusions.