Action of Calcium Slow Channel Inhibitors on Cardiac and Vascular Smooth Muscle Membranes

Abstract

Cardiac and most vascular smooth muscle cells depend on extracellular Ca²⁺ for contraction. The influx of Ca²⁺ in these cells is known to occur through Ca²⁺-selective slow channels during the phase 2 of the action potential when these channels are presumably “open.” A number of organic compounds classified as calcium antagonists (1) were found to antagonize the extracellular Ca²⁺-dependent contraction. These compounds are also referred to as “calcium slow channel inhibitors,” “calcium channel blockers,” or “calcium entry blockers.” While they differ in chemical structures (Fig. 1), they do exert at least one common effect, viz., inhibition of contraction or relaxation in cardiac and vascular smooth muscles. They are much more potent in vascular smooth muscle than in cardiac muscle, producing vasodilation at low concentrations and negative inotropy at much higher concentrations. By virtue of this differential effect, some of these calcium antagonists have been found to be useful in the treatment of angina pectoris.