Calcium channels in smooth muscle. Properties and regulation.
Calcium channels in smooth muscle. Properties and regulation.
复制标题
平滑肌中的钙通道。
DOI：
10.1111/j.1749-6632.1989.tb24099.x
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发表时间：
1989
影响因子：
5.2
通讯作者：
Triggle,AM
中科院分区：
文献类型：
--
作者：
Triggle,DJ;Zheng,W;Hawthorn,M;Kwon,YW;Wei,XY;Joslyn,A;Ferrante,J;Triggle,AM
Smooth muscle is homogenous in neither function nor physical characteristics, and it has been remarked, with some asperity,“that the most constant property of smooth muscle 1s its variability.” It is agreed, however, that a key component of tension development in smooth muscle is an elevation of intracellular Ca” subsequent to chemical, electrical, or mechanical stimulation. In this respect smooth muscle behaves similarly to cardiac and skeletal muscle and to motile systems generally. However, important differences do exist between smooth and other muscle systems in the control processes by which elevation of intracellular Ca” from a resting level of approximately lo-* M to a stimulated level of approximately 5 X 10-’M is linked to tension development. Additionally, smooth muscle is capable both of generating rapid responses and of sustaining prolonged periods of tension (tone). Determination of the control processes regulating Ca2+ mobilization in smooth muscle, both visceral and vascular, must accommodate these characteristics of tension development. A widely accepted hypothesis holds that Ca”-calmodulin (CM) activation of myosin light chain kinase leads to the phosphorylation of myosin light chain which, in its phosphorylated form, interacts with actin. A cycling actin-myosin cross-bridge process is presumed to underlie tension development (for review see Kamm and Stull’). A more recently developed alternative hypothesis holds that the processes underlying the generation and maintenance of tension in smooth muscle may be quite different? The initial component of response is assumed to involve the CM-dependent activation of myosin light chain kinase and the sustained component of response is postulated to occur through Caz+ activation of membrane-associated protein kinase C by the diacylglycerol formed in the receptor-initiated, phospholipase C mediated breakdown
