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血管平滑肌收缩性中的钙调节

Calcium regulation in vascular smooth muscle contractility.

作者信息

Johns A, Leijten P, Yamamoto H, Hwang K, van Breemen C

出版信息

Am J Cardiol. 1987 Jan 23;59(2):18A-23A. doi: 10.1016/0002-9149(87)90171-8.

DOI:10.1016/0002-9149(87)90171-8
PMID:2433925
Abstract

The contractile activity of vascular smooth muscle is regulated by control over the cytoplasmic calcium concentration. The intracellular calcium receptor is calmodulin, which, through stimulation of myosin light chain kinase, can activate 2 different contractile states. The calcium is supplied from the sarcoplasmic reticulum and the extracellular space; a minor component is supplied from the inner surface of the plasmalemma. The main intracellular messenger responsible for the transduction of receptor occupation and calcium release from the sarcoplasmic reticulum is IP3 and, to a lesser extent, calcium itself. The superficial location of the sarcoplasmic reticulum in vascular smooth muscle makes it the logical area for control of calcium entry due to calcium leak or through either or both types of calcium channel. The sarcoplasmic reticulum, therefore, acts as a "superficial calcium buffer barrier" and is probably the major system controlling free cytoplasmic calcium concentration in vascular smooth muscle.

摘要

血管平滑肌的收缩活动受细胞质钙浓度的调控。细胞内钙受体是钙调蛋白,它通过刺激肌球蛋白轻链激酶,可激活两种不同的收缩状态。钙由肌浆网和细胞外间隙提供;一小部分由质膜内表面提供。负责转导受体占据信号以及从肌浆网释放钙的主要细胞内信使是肌醇三磷酸(IP3),钙本身的作用相对较小。肌浆网在血管平滑肌中的浅表位置使其成为因钙泄漏或通过一种或两种钙通道控制钙内流的合理区域。因此,肌浆网充当“浅表钙缓冲屏障”,可能是控制血管平滑肌细胞质游离钙浓度的主要系统。

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Calcium regulation in vascular smooth muscle contractility.血管平滑肌收缩性中的钙调节
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