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-mu-g . 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.