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神经肽Y(NPY)引起冠状动脉血管收缩所涉及的效能和受体。

Potency and receptors involved in coronary vasoconstriction caused by neuropeptide Y(NPY).

作者信息

Aizawa Y, Satoh M, Aizawa M, Funazaki T, Niwano S, Miyajima S, Shibata A

机构信息

First Department of Internal Medicine, Niigata University School of Medicine, Japan.

出版信息

Jpn Heart J. 1987 Nov;28(6):891-8. doi: 10.1536/ihj.28.891.

DOI:10.1536/ihj.28.891
PMID:2832630
Abstract

Using anesthetized dogs, the coronary vascular effects of neuropeptide Y (NPY) were studied and the action of alpha- or serotonergic receptor blockade on the action of NPY was evaluated. To demonstrate the biological significance of the action of NPY, the vasoconstrictor potencies of NPY and norepinephrine were compared. One to 5 nmol of intracoronary NPY reduced coronary flow in a dose-dependent manner. The action started rather gradually and lasted for 10 min or more. Since perfusion pressure and central venous pressure were unchanged, the decrease in coronary flow should be a result of coronary vasoconstriction. Intracoronary norepinephrine infusion caused vasodilatation but when dogs were pretreated with 0.5 to 1.0 mg/kg of systemic propranolol, a vasoconstrictor effect was observed at a 5 times higher dose than with NPY. Furthermore, the action of NE was only transient, lasting for 30 sec or less. The vasoconstrictor action of NPY was not antagonized by phentolamine or by ketanserin. Since NPY is an endogenous polypeptide found in the sympathetic nerve terminals around coronary arteries, it may participate in the regulation of coronary flow.

摘要

利用麻醉犬,研究了神经肽Y(NPY)对冠状动脉血管的作用,并评估了α受体或5-羟色胺能受体阻断剂对NPY作用的影响。为了证明NPY作用的生物学意义,比较了NPY和去甲肾上腺素的血管收缩效力。冠状动脉内注射1至5 nmol的NPY可使冠状动脉血流量呈剂量依赖性减少。这种作用开始较为缓慢,持续10分钟或更长时间。由于灌注压和中心静脉压未发生变化,冠状动脉血流量的减少应是冠状动脉血管收缩的结果。冠状动脉内注射去甲肾上腺素可引起血管舒张,但当犬用0.5至1.0 mg/kg的全身性普萘洛尔预处理后,观察到产生血管收缩作用的剂量比NPY高5倍。此外,NE的作用只是短暂的,持续30秒或更短时间。NPY的血管收缩作用未被酚妥拉明或酮色林所拮抗。由于NPY是一种存在于冠状动脉周围交感神经末梢的内源性多肽,它可能参与冠状动脉血流量的调节。

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