ORIGINAL ARTICLE: PDF OnlyKahan Thomas; Pernow, John; Schwieler, Jonas; Lundberg, Jan M.; Hjemdahl, Paul; Wallin, B. GunnarJournal of Hypertension: December 1988 - p S532-534 Buy Abstract The possibility that neuropeptide Y, a vasoconstrictor peptide co-stored with noradrenaline in sympathetic nerves, participates in neurogenic vascular control was investigated in canine gracilis muscle in situ. Sympathetic nerve stimulation with recordings of the normal irregular sympathetic discharge to human skeletal muscle elicited frequency-dependent overflows of neuropeptide Y-like immunoreactivity and noradrenaline, and vasoconstriction. The overflow of neuropeptide Y-like immunoreactivity was more markedly enhanced with increasing frequency. Exogenous neuropeptide Y reduced nerve stimulation-evoked noradrenaline overflow, possibly through a prejunctional mechanism, and caused dose-dependent vasoconstriction. Nerve stimulation elicited significant vasoconstrictor responses following α- and β-adrenoceptor blockade with phenoxybenzamine and propranolol, which abolished the vasoconstriction to exogenous noradrenaline. Nerve stimulation-evoked overflows of neuropeptide Y-like immunoreactivity and noradrenaline were enhanced, consistent with prejunctional α-adrenoceptor-mediated inhibition of the release. Thus, neuropeptide Y is likely to be involved in the non-adrenergic component of vasoconstriction, and may participate in the physiological control of vascular tone at moderate to high impulse frequencies. © Lippincott-Raven Publishers.