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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Vasodilation in human subcutaneous arteries induced by neuropeptide Y is mediated by neuropeptide Y Y1 receptors and is nitric oxide dependent.
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Vasodilation in human subcutaneous arteries induced by neuropeptide Y is mediated by neuropeptide Y Y1 receptors and is nitric oxide dependent.

机译：由神经肽Y诱导的人皮下动脉血管舒张由神经肽Y Y1受体介导，并且是一氧化氮依赖性的。

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摘要

Neuropeptide Y (NPY) is known as a potent vasoconstrictor of peripheral blood vessels both in vivo and in vitro. There have been reports suggesting that NPY also has a dilatory effect. The aim of the present study was to elucidate whether NPY dilates small human subcutaneous arteries. Subcutaneous arteries, obtained from patients undergoing abdominal surgery, were mounted in in vitro tissue baths, and the vascular responses to NPY were investigated. The presence of mRNA encoding the human NPY Y1 receptor in endothelial cells from human umbilical veins was studied by the use of reverse transcriptase - polymerase chain reaction (RT-PCR). In arteries precontracted with the prostaglandin analogue U46619, NPY induced a concentration-dependent vasodilation (Emax 30 +/- 10% of the U46619-induced contraction), which was significantly inhibited by the NPY Y1 receptor antagonist BIBP3226 (1 microM), causing a rightward shift of the concentration-response curve, pEC50 7.1 +/- 0.3 vs. 7.7 +/- 0.3 for NPY alone. After pretreatment with the nitric oxide synthetase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) (10 microM), the dilation was abolished (Emax 6 +/- 5% of the U46619-induced contraction). mRNA encoding the human NPY Y1 receptor was detected in endothelial cells from human umbilical veins. It was concluded that NPY induces vasodilation in human subcutaneous arteries. The dilation is mediated via the NPY Y1 receptor and is dependent on nitric oxide.
机译：神经肽Y（NPY）在体内和体外均被认为是外周血管的有效血管收缩剂。有报道表明NPY也具有扩张作用。本研究的目的是阐明NPY是否会扩张人的皮下小动脉。从进行腹部手术的患者获得的皮下动脉安装在体外组织浴中，并研究了对NPY的血管反应。通过使用逆转录酶-聚合酶链反应（RT-PCR），研究了人脐静脉内皮细胞中编码人NPY Y1受体的mRNA的存在。在与前列腺素类似物U46619预收缩的动脉中，NPY诱导了浓度依赖性的血管舒张作用（Emax为U46619诱导的收缩的最大30 +/- 10％），该作用被NPY Y1受体拮抗剂BIBP3226（1 microM）显着抑制。浓度-响应曲线的右移，pEC50 7.1 +/- 0.3与单独NPY的7.7 +/- 0.3。用一氧化氮合成酶抑制剂N（G）-硝基-L-精氨酸甲酯（L-NAME）（10 microM）预处理后，消除了膨胀作用（Emax 19-诱导的收缩的Emax 6 +/- 5％）。在人脐静脉内皮细胞中检测到编码人NPY Y1受体的mRNA。结论是NPY诱导人皮下动脉血管舒张。扩张是通过NPY Y1受体介导的，取决于一氧化氮。

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