Isolated longitudinal smooth muscle from guinea pig ileum exposed to a high potassium depolarizing medium exhibited a sustained increase in muscle tone and an increase in potassium efflux. When the concentration of calcium ion in the medium was elevated the increase in muscle tone was enhanced, but the change in potassium efflux was reduced slightly. Lowering the calcium concentration diminished the increase in muscle tone. Both cocaine and ethanol completely inhibited the sustained contraction of potassium-depolarized fibers. Addition of excess calcium ion reversed these inhibitions. Cocaine acted primarily like a competitive antagonist; and ethanol, like an indirect antagonist of calcium, ion. Under certain conditions acetylcholine potentiated the reversal by calcium ion of the drug-induced inhibitions. The two inhibitory drugs had dissimilar effects on potassium efflux from smooth muscle fibers immersed in Tyrode solution. Cocaine depressed and ethanol enhanced this membrane process. However, the increase in potassium efflux induced by acetylcholine was inhibited by ethanol. This inhibition also was reversed by increasing the concentration of calcium ion in the medium. The data suggested that calcium activates and cocaine and ethanol inhibit a cellular reaction which occurs beyond the point of membrane depolarization and is essential for smooth muscle contraction. Furthermore, calcium serves to depress membrane excitability, but appears to have a specific stimulatory role in the acetylcholine-induced increase in potassium efflux from longitudinal fibers.

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