Potency and receptors involved in coronary vasoconstriction caused by neuropeptide Y(NPY).

Using anesthetized dogs, the coronary vascular effects of neuropeptide Y (NPY) were studied and the action of alpha- or serotonergic receptor blockade on the action of NPY was evaluated. To demonstrate the biological significance of the action of NPY, the vasoconstrictor potencies of NPY and norepinephrine were compared. One to 5 nmol of intracoronary NPY reduced coronary flow in a dose-dependent manner. The action started rather gradually and lasted for 10 min or more. Since perfusion pressure and central venous pressure were unchanged, the decrease in coronary flow should be a result of coronary vasoconstriction. Intracoronary norepinephrine infusion caused vasodilatation but when dogs were pretreated with 0.5 to 1.0 mg/kg of systemic propranolol, a vasoconstrictor effect was observed at a 5 times higher dose than with NPY. Furthermore, the action of NE was only transient, lasting for 30 sec or less. The vasoconstrictor action of NPY was not antagonized by phentolamine or by ketanserin. Since NPY is an endogenous polypeptide found in the sympathetic nerve terminals around coronary arteries, it may participate in the regulation of coronary flow.