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关于组胺能机制在血管紧张素II对兔主动脉和大鼠肺作用中的证据。

Evidence for a histaminergic mechanism on the effects of angiotensin II in the rabbit aorta and rat lung.

作者信息

Zengil H

出版信息

Arch Int Pharmacodyn Ther. 1981 Jul;252(1):67-71.

PMID:7305553
Abstract

The influence of a histidine decarboxylase (HD) inhibitor, GYKI 11.121, on the action of angiotension II (AII) was investigated in the isolated continuously superfused rabbit aortic strip and perfused rat lung. An A II analog, Sar1-Ile5-A II, was also used only in aortic strip experiments. The myotropic effects of both peptides on the rabbit aorta were found to be inhibited when GYKI 11.121 was added to the superfusion medium. However, the vasoconstrictor effect of A II was found to be enhanced in the isolated rat lung following the addition of GYKI 11.121 to the perfusion medium. These findings are explained by the presence of a histaminergic component in the myotropic action of A II peptides.

摘要

在离体持续灌流的兔主动脉条和灌流的大鼠肺中,研究了组氨酸脱羧酶(HD)抑制剂GYKI 11.121对血管紧张素II(AII)作用的影响。仅在主动脉条实验中还使用了一种AII类似物Sar1-Ile5-AII。当向灌流介质中添加GYKI 11.121时,发现这两种肽对兔主动脉的肌性效应均受到抑制。然而,在向灌流介质中添加GYKI 11.121后,发现离体大鼠肺中AII的血管收缩效应增强。这些发现可以用AII肽的肌性作用中存在组胺能成分来解释。

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