Neuropeptide Y-induced pressor responses: activation of a non-adrenergic mechanism, potentiation by reserpine and blockade by nifedipine.

Intravenous administration of neuropeptide Y (NPY) to pentobarbital anesthetized rats produced a short-lasting concentration-dependent increase in systolic and diastolic blood pressure. Pretreatment of rats with 2 mg/kg reserpine potentiated the NPY-induced pressor responses causing a leftward shift of the NPY concentration-response curve. In addition, reserpinization lengthened the duration of the NPY pressor effects. Reserpine also potentiated the noradrenaline-induced pressor effect but not that caused by angiotensin II. The NPY-induced increase in blood pressure was not antagonized by phenoxybenzamine. On the contrary, some degree of potentiation was observed, particularly with the larger doses of NPY. The NPY pressor responses were reduced by nifedipine in control and in reserpinized rats. The results demonstrate that the NPY-induced pressor responses were not related to adrenergic mechanisms. NPY may activate calcium channels in the cardiovascular system to promote an influx of calcium, causing peripheral vasoconstriction.