Evidence that neuropeptide Y released from noradrenergic axons causes prolonged contraction of the guinea-pig uterine artery.

The participation of neuropeptide Y (NPY) in transmission from sympathetic vasoconstrictor neurons was investigated in the guinea-pig uterine artery, where NPY has been demonstrated immunohistochemically in noradrenergic axons. Exogenous NPY produced long-lasting contractions of isolated arterial segments at low resting tone. Low concentrations of NPY (10(-8)-3 X 10(-7) mol.l-1) were more potent than equimolar concentrations of noradrenaline (NA). NPY produced concentration-dependent desensitization to further application of NPY, but did not affect the magnitude of NA contractions. Trypsin (1.4-2 micrograms.ml-1) reduced NPY-induced contractions by 80-100%, but did not alter NA-induced contractions. Transmural electrical stimulation of arterial segments, after surgical removal of vasodilator axons, produced biphasic contractions which were abolished by guanethidine. Prazosin abolished the fast phase of the neurogenic contraction, leaving a slow contraction with a time course similar to that produced by a low concentration of NPY. The slow contraction was more pronounced at higher frequencies of stimulation (15-20 Hz) than at lower frequencies, and was selectively reduced after desensitization produced by NPY (10(-5) mol.l-1), or after exposure to trypsin. These results suggest that sympathetic vasoconstriction of the guinea-pig uterine artery is produced by release of both NA and NPY from noradrenergic axons.