Endothelium-independent potentiation by neuropeptide Y of vasoconstrictor responses in isolated arteries from rat and rabbit.

An endothelium-dependent action of neuropeptide Y (NPY) has been implicated in studies on various vascular beds. In the present study, the requirement of an intact endothelium for NPY-evoked potentiation of the response to sympathetic nerve stimulation was determined in the small mesenteric arteries of the rat and in the central ear artery of the rabbit. Further, NPY-mediated inhibition of relaxing influences was determined in small mesenteric arteries of the rat. Vascular segments were mounted in a double myograph, where one of the two suspended vessels was denuded of endothelium by gently rubbing the intimal surface. Removal of endothelium was verified by en-face silver staining. In both species, the response to bursts of transmural field stimulation eliciting 10% of maximal contraction was potentiated 2-4 times in the presence of 10 nM NPY, whether the endothelium was present or not. In small mesenteric arteries precontracted with noradrenaline, addition of acetylcholine (I microM) caused relaxation only in vessels with an intact endothelium. Subsequent addition of 10 nM NPY enhanced vasoconstriction in both intact and endothelium-denuded vessels. The endothelium-independent beta-adrenergic agonist isoprenaline (I microM) relaxed both intact and denuded small mesenteric arteries, and in both further addition of 10 nM NPY increased the contraction to about the same extent. The results demonstrate that NPY potentiates the responses to sympathetic field stimulation in small mesenteric arteries from the rat and in central ear artery from rabbit whether the endothelium is present or not. NPY inhibits both endothelium-dependent and -independent relaxations in small mesenteric arteries from rat.