Neuropeptide Y increases force development through a mechanism that involves calcium entry in resistance arteries.

Abstract

The hypothesis that neuropeptide Y (NPY) potentiates noradrenaline (NA)-induced vascular force development by increasing free intracellular Ca2+ ([Ca2+]i) was tested in rat mesenteric resistance arteries. NPY (100 nM) alone was not able to increase either the contraction or [Ca2+]i. However, pretreatment of mesenteric resistance arteries with 100 nM NPY potentiated both [Ca2+]i and active stress induced by 1.5 microM NA. Addition of 100 nM NPY to vessels that had been precontracted with NA (1.5 microM) elicited a large increase in [Ca2+]i and an increase in active stress development. In Ca(2+)-free medium containing 2 mM ethylene glycol-bis(beta-aminoethyl ether) N,N,N',N'-tetraacetic acid, the potentiating effect of NPY on the NA-induced contraction was prevented, and readdition of Ca2+ resulted in a large increase in both [Ca2+]i and active stress development. It is concluded that NPY potentiates NA-induced contraction in the isolated mesenteric resistance artery by inducing a rise in [Ca2+]i through an influx of Ca2 from the extracellular source.