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The studies were performed on the rat portal vein smooth muscle cells, using double sucrose-gap method. 10(-9)--10(-7) M-verapamil was shown to selectively block the tonic component of potassium contracture. Since potassium depolarization of the membrane persists, it may evidence that verapramil had a specific effect on the excitation-contraction coupling by blocking the passive calcium entry into the muscle cells. At higher concentrations (10(-6)--10(-5) M) verapramil produced inhibition of the phasic component of potassium contracture by blocking the potential-dependent calcium canals of the portal vein smooth muscle cell membrane responsible for generation of the action potentials.
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