Mechanisms underlying pre- and postjunctional effects of neuropeptide Y in sympathetic vascular control.

摘要: The effects of porcine neuropeptide Y (NPY) regarding sympathetic vascular control were studied in vitro on isolated rat blood vessels. 10 -9 M NPY enhanced (about two-fold) the contractile responses to transmural nerve stimulation (TNS), noradrenaline (NA) and adrenaline femoral artery. Higher concentrations (> 10-8 M) caused an adrenoceptor-resistant contraction per se. TNS-evoked [3H]NA efflux was significantly reduced by a concentration-dependent manner (threshold M). calcium antagonist, nifedipine, abolished NPY-induced enhancement NA contractions but did not influence prejunctional inhibition release. Receptor-binding studies showed that ratio alpha1- alpha2-adrenoceptors artery 30:1. cause any detectable change number or alpha2-adrenoceptor binding sites affinity alpha2-binding sites, as revealed prazosin- clonidine-binding, respectively. also inhibited release (by 42–86%) superior mesenteric basilar arteries portal veins. still depressed secretion from vein presence phentolamine. clear-cut artery, increased force spontaneous vein, while only weak observed vein. NA-induced markedly slightly uninfluenced In conclusion, all vessels tested, depresses via nifedipine-resistant action. Furthermore, exerts variable, Ca2+-dependent vasoconstrictor effect TNS contractions.