Abstract
The ability of analogues of neuropeptide Y (NPY) to produce direct vasoconstriction, or to antagonize NPY constrictions, was examined in isolated segments of the thoracic vena cava and the uterine artery of guinea-pigs, where NPY mediates a slow phase of sympathetic vasoconstriction. [Leu 31,Pro 34]NPY, NPY(13–36) and NPY(18–36) all contracted the uterine artery and the vena cava. Contractions produced by [Leu 31,Pro 34]NPY were similar in time course to those produced by porcine NPY (pNPY), although contractions produced by NPY(13–36) or NPY(18–36) typically were slower than pNPY contractions. In both vessels the order of potency of the agonists was pNPY ≥ [Leu 31,Pro 34]NPY > NPY(13–36) > NPY(18–36). High concentrations (10 −5mol.l −1) of pNPY or [Leu 31,Pro 34]NPY produced desensitization of contractions of the uterine artery produced by NPY(13–36). The reported NPY receptor antagonists, PYX-1 and PYX-2 (5 × 10 −6mol.l −1), slightly reduced (by 21–47%) the magnitude of constrictions produced by exogenous pNPY (1–3 × 10 −8 mol.l −1) in both the uterine artery and the vena cava. These results show that the NPY receptors mediating slow sympathetic vasoconstriction of both the uterine artery and the vena cava are likely to be predominantly Y 1 receptors, despite differences between the adrenoceptors mediating sympathetic responses in the two blood vessels.
Published Version
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