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Effects of neuropeptide Y on the response of isolated blood vessels to norepinephrine and sympathetic field stimulation.

1989; American Society for Pharmacology and Experimental Therapeutics; Volume: 250; Issue: 2 Linguagem: Inglês

10.1016/s0022-3565(25)22241-8

1521-0103

J. Paul Hieble, John G. Duesler, Robert Daly,

Eicosanoids and Hypertension Pharmacology

Although neuropeptide Y (NPY) is not a potent vasoconstrictor in many vascular beds, nanomolar concentrations of this peptide can potentiate the response of isolated blood vessels to sympathetic stimulation or exogenous vasoconstrictors. In the isolated perfused rabbit ear artery, NPY produces a concentration-related potentiation of the response to field stimulation. The potency of NPY in inducing potentiation of nerve-mediated vasoconstriction was not dependent on whether the NPY was administered intra- or extraluminally. In these perfused vessels the endothelium was intact. Similar potentiation of the response to field stimulation is also observed in superfused ring segments of rabbit ear artery, provided that the endothelium was not damaged mechanically. The response to field stimulation in the rabbit ear artery is mediated by the alpha-1 adrenoceptor; in contrast, stimulation induced contraction in the canine saphenous vein results from the activation of vascular alpha-2-adrenoceptors. Despite this difference, the effect of NPY in ring segments of canine saphenous vein was similar to that observed in the ear artery. NPY also produced an endothelium-dependent potentiation of the constrictor response to exogenous norepinephrine in superfused segments of both ear artery and saphenous vein. Although the NPY-induced potentiation of stimulation-induced vasoconstriction was not inhibited by indomethacin, suggesting that an arachidonic acid metabolite is not involved, the release of another endothelial-derived vasoconstrictor substance, as yet unidentified, by NPY may explain its ability to potentiate the responses to both nerve stimulation and a variety of exogenous vasoconstrictors.