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亮氨酸脑啡肽可引发纳洛酮不敏感的肺血管收缩。

Leu-enkephalin provokes naloxone-insensitive pulmonary vasoconstriction.

作者信息

Gillespie M N, Bowdy B D, Reinsel C N, Iwamoto E T, Crooks P A

出版信息

Life Sci. 1984 Mar 19;34(12):1177-83. doi: 10.1016/0024-3205(84)90090-0.

DOI:10.1016/0024-3205(84)90090-0
PMID:6708723
Abstract

Leu-enkephalin evoked dose-dependent pulmonary vasoconstriction in isolated perfused rat lungs. The pressor responses were not attenuated by either naloxone or naltrexone nor were they mimicked by morphine. Blockade of histamine receptors with pyrilamine or blockade of serotonin receptors with methysergide also failed to antagonize leu-enkephalin-induced pulmonary vasoconstrictor responses. These results suggest that neither opiate, histamine, nor serotonin receptors are involved with the pressor effects of leu-enkephalin on the pulmonary circulation. We propose that leu-enkephalin may have direct vasoconstrictor effects on the pulmonary circulation of isolated perfused rat lungs that may not be mediated by conventional opiate receptors.

摘要

亮脑啡肽在离体灌注的大鼠肺中引起剂量依赖性的肺血管收缩。纳洛酮或纳曲酮均未减弱其升压反应,吗啡也不能模拟该反应。用吡苄明阻断组胺受体或用麦角新碱阻断5-羟色胺受体也不能拮抗亮脑啡肽诱导的肺血管收缩反应。这些结果表明,阿片、组胺和5-羟色胺受体均不参与亮脑啡肽对肺循环的升压作用。我们提出,亮脑啡肽可能对离体灌注大鼠肺的肺循环有直接的血管收缩作用,这种作用可能不是由传统的阿片受体介导的。

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