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 receptor 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.
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