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神经肽Y(NPY)可能通过激活NPY1受体来抑制小鼠心房的自发收缩。

Neuropeptide Y (NPY) inhibits spontaneous contraction of the mouse atrium by possible activation of the NPY1 receptor.

作者信息

Oki Y, Teraoka H, Kitazawa T

机构信息

Department of Veterinary Medicine, Rakuno Gakuen University, Ebetsu, Hokkaido, Japan.

出版信息

Auton Autacoid Pharmacol. 2017 Mar;37(2):23-28. doi: 10.1111/aap.12055.

DOI:10.1111/aap.12055
PMID:28544313
Abstract

Neuropeptide Y (NPY) causes various central and peripheral actions through activation of G-protein-coupled NPY receptors. Although a species-dependent difference in cardiac actions of NPY has been reported, the responses to NPY have not been examined in mice, widely used experimental animals. This study aimed to clarify the responses to NPY and the receptor subtype involved in the responses in mouse atrium. Neuropeptide Y caused negative inotropic and negative chronotropic actions in spontaneous beating right atria. Negative inotropic actions were more marked than negative chronotropic actions. Therefore, negative inotropic actions were studied in detail for evaluation of the NPY-induced cardiac actions in mouse atrium. Neuropeptide Y-induced negative inotropic actions were not affected by atropine but were abolished in the atria from pertussis toxin-treated mice. In isolated atrial preparations from reserpine-treated mice, NPY-induced negative inotropic actions were significantly attenuated. [Leu31, Pro34]-NPY, but not peptide YY, was effective in decreasing spontaneous contraction in atrial preparations. Although Y , Y , Y and Y receptor mRNAs were expressed almost equally in the brain, NPY receptor mRNA was dominantly expressed in the atrium. In conclusion, NPY caused negative inotropic and chronotropic actions through activation of the Y receptor in the mouse atrium. A high expression level of Y mRNA in the atrium suggests a functional role of NPY in the regulation of mouse cardiac contraction.

摘要

神经肽Y(NPY)通过激活G蛋白偶联的NPY受体引起多种中枢和外周作用。尽管已报道NPY在心脏作用方面存在物种依赖性差异,但尚未在广泛使用的实验动物小鼠中研究其对NPY的反应。本研究旨在阐明小鼠心房对NPY的反应以及参与这些反应的受体亚型。神经肽Y在自发性搏动的右心房中引起负性肌力和负性变时作用。负性肌力作用比负性变时作用更明显。因此,为评估NPY诱导的小鼠心房心脏作用,对负性肌力作用进行了详细研究。神经肽Y诱导的负性肌力作用不受阿托品影响,但在百日咳毒素处理的小鼠心房中被消除。在利血平处理的小鼠分离心房标本中,NPY诱导的负性肌力作用明显减弱。[Leu31,Pro34]-NPY而非肽YY能有效降低心房标本中的自发性收缩。尽管Y1、Y2、Y4和Y5受体mRNA在脑中几乎等量表达,但NPY受体mRNA在心房中占主导表达。总之,NPY通过激活小鼠心房中的Y受体引起负性肌力和负性变时作用。心房中Y mRNA的高表达水平提示NPY在调节小鼠心脏收缩中具有功能作用。

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