Bohr D F, Webb R C
Am J Med. 1984 Oct 5;77(4A):3-16. doi: 10.1016/s0002-9343(84)80032-7.
The contractile state of vascular smooth muscle influences arterial blood pressure and regulates organ blood flow. Current evidence suggests that the contractile apparatus of vascular smooth muscle is composed of thin and thick filaments, and that force generated between these two filaments provides the mechanism for cell shortening. The molecular events that initiate the interaction between these filaments are dependent upon the free sarcoplasmic concentration of activator calcium, which is regulated by the cell membrane and at subcellular sites. Changes in electrical activity of the cell membrane and interaction of pharmacologic agents with membrane receptors alter the cell, causing either a decrease or increase in sarcoplasmic calcium concentration and thus changing the contractile state of the vascular smooth muscle cell. Alterations in the cellular mechanisms that regulate intracellular calcium concentration may contribute to abnormal vascular function in pathologic states. In this brief review, the normal mechanism of vascular smooth muscle contraction is described, and the evidence that indicates that components of the contractile process change in hypertension is examined.
血管平滑肌的收缩状态影响动脉血压并调节器官血流。目前的证据表明,血管平滑肌的收缩装置由细肌丝和粗肌丝组成,这两种肌丝之间产生的力量为细胞缩短提供了机制。引发这些肌丝间相互作用的分子事件取决于激活钙的游离肌浆浓度,该浓度由细胞膜和亚细胞位点调节。细胞膜电活动的变化以及药物制剂与膜受体的相互作用会改变细胞,导致肌浆钙浓度降低或升高,从而改变血管平滑肌细胞的收缩状态。调节细胞内钙浓度的细胞机制改变可能导致病理状态下血管功能异常。在这篇简短的综述中,描述了血管平滑肌收缩的正常机制,并审视了表明收缩过程的组成部分在高血压中发生变化的证据。