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BIBP3226 inhibits neuropeptide Y and pancreatic polypeptide potentiated neurogenic vasoconstriction.

机译:BIBP3226抑制神经肽Y和胰腺多肽增强的神经源性血管收缩。

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摘要

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.
机译:神经肽Y(NPY)增强大鼠尾动脉对体外肾上腺素能神经的收缩反应。 NPY Y1选择性拮抗剂BIBP3226((R)-N2-(二苯基乙酰基)-N-[(4-羟苯基)甲基]-精氨酸)抑制NPY在大鼠尾动脉制剂中的血管作用(IC50 = 126 nM)。 BIBP3226还抑制了选择性Y1激动剂[Leu31,Pro34] NPY的作用,并完全取消了禽胰腺多肽的作用,该多肽在该制剂中能够增强神经源性血管收缩。这些作用是可逆的,最有可能是由Y1受体亚型介导的,因为我们未能观察到大鼠尾动脉中Y2受体亚型的任何功能证据。尾动脉为NPY和NPY拮抗剂的药理分析提供了有用的功能测定。

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