The potentiating effects of neuropeptide Y on vascular smooth muscle.

In the present study, the roles of nifedipine-sensitive calcium channels and the endothelium in the potentiating effect of neuropeptide Y (NPY) in the rat tail artery were investigated. Contractile responses to KCl, $\alpha,\beta$-methylene ATP (mATP), and NA were compared. KCl- and mATP-induced vasoconstriction is closely linked to nifedipine-sensitive calcium channels while NA-induced vasoconstriction is not. The role of the endothelium in potentiating effects of NPY was also tested by comparing intact arterial ring segments with denuded arterial ring segments. Freshly isolated single smooth muscle cells in which the influences of the endothelium and the nerves were unequivocally eliminated were examined to verify the results of the ring segments. Contractile responses to KCl and mATP were potentiated by NPY (50 nM) while NA responses were not potentiated at 50 nM but were at 500 nM NPY. The potentiating effect of NPY was antagonized by nifedipine. The intact and denuded arteries responded similarly. The shortening of single smooth muscle cells in response to KCl and mATP was potentiated by NPY (50 nM) while the noradrenaline response was potentiated by NPY at 500 nM but not at 50 nM. (Abstract shortened by UMI.