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[缺氧时血管平滑肌细胞质膜钙通透性变化的机制]

[Mechanism of changes in the calcium permeability of the sarcolemma of vascular smooth muscle cells during hypoxia].

作者信息

Solov'ev A I, Stefanov A V

出版信息

Fiziol Zh SSSR Im I M Sechenova. 1985 Dec;71(12):1560-7.

PMID:4092776
Abstract

In isolated preparations of smooth muscle of the rat portal vein, removal of Ca2+ from perfusate or addition of Ca2+--antagonists as well as hypoxia entailed inhibition of vascular smooth muscle contractile activity. Uptake of 45Ca by vascular smooth muscle cells was diminished in hypoxia. Liposomes filled with Ca2+ or Cr but not ATP prevented the hypoxic relaxation of vascular smooth muscle. One of the main reasons of the decrease of vascular smooth muscle contractility in hypoxia seems to be the disturbance of calcium channel phosphorylation and the decrease of sarcolemma calcium permeability.

摘要

在大鼠门静脉平滑肌的离体标本中,从灌注液中去除Ca2+或添加Ca2+拮抗剂以及缺氧都会导致血管平滑肌收缩活性受到抑制。缺氧时血管平滑肌细胞对45Ca的摄取减少。填充有Ca2+或Cr而非ATP的脂质体可防止血管平滑肌的缺氧性舒张。缺氧时血管平滑肌收缩性降低的主要原因之一似乎是钙通道磷酸化紊乱和肌膜钙通透性降低。

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