Pertussis toxin attenuates postsynaptic actions of neuropeptide Y on the guinea-pig uterine artery.

The mechanisms by which neuropeptide Y (NPY) mediates its postsynaptic actions on the guinea-pig uterine artery, were investigated by incubating arterial segments in culture medium containing pertussis toxin (PTX). Arteries were incubated with 0, 0.25 or 1 microgram.ml-1 PTX for 24 or 48 h. Arterial segments incubated in culture medium without PTX showed the three postsynaptic responses to NPY which were reported previously in uncultured arteries: NPY further contracted segments which were precontracted with prostaglandin F2 alpha; NPY reduced the maximum relaxations produced by vasoactive intestinal peptide (VIP); and NPY produced a rightward shift in the VIP concentration-response curves. PTX attenuated the three actions of NPY on the uterine artery to different degrees. PTX also reduced the magnitude of contractions produced by prostaglandin F2 alpha, but did not affect contractions produced by 0.126 M KCl, or relaxations produced by VIP in the absence of NPY. These data indicate that all postsynaptic actions of NPY on the uterine artery, and contractions produced by prostaglandin F2 alpha, are at least partly mediated by pertussis toxin-sensitive GTP-binding proteins. It is not clear whether these multiple actions of NPY are mediated by one, or more than one, GTP-binding protein.