BIBP3226 inhibits neuropeptide Y and pancreatic polypeptide potentiated neurogenic vasoconstriction.

Abstract

Neuropeptide Y (NPY) potentiates the contractile response of the rat caudal artery to adrenergic nerve stimulation in-vitro. The NPY Y1 selective antagonist BIBP3226 ((R)-N2-(diphenylacetyl)-N-[(4-hydroxyphenyl)methyl]-argininami de), inhibited the vascular effects of NPY in rat caudal artery preparations in-vitro (IC50 =126 nM). BIBP3226 also inhibited the effects of the selective Y1 agonist [Leu31,Pro34]NPY and completely abolished the effects of avian pancreatic polypeptide that was shown to be capable of potentiating neurogenic vasoconstriction in this preparation. These effects were reversible and are most likely mediated by the Y1 receptor subtype since we failed to observe any functional evidence of a Y2 receptor subtype in rat caudal artery. The caudal artery provides a useful functional assay for pharmacological analysis of NPY and NPY antagonists.

Cite this paper

@article{Barrios1998BIBP3226IN, title={BIBP3226 inhibits neuropeptide Y and pancreatic polypeptide potentiated neurogenic vasoconstriction.}, author={Victor E Barrios and Allyson G. Nelson and Candice F. Toombs}, journal={Life sciences}, year={1998}, volume={62 6}, pages={525-32} }