Certain twitch-potentiating agents enhance caffeine-contracture tension in frog toe muscle, likely through actions at the external surface of the plasma membrane.
Observations in frog skeletal muscle warrant no clinical translation; leaves open membrane mechanisms for cardiac models.
Submaximum caffeine-contracture tension in frog toe muscle was enhanced by a number of twitch-potentiating agents (chloroform, pentobarbital, quinidine, nitrate, perchlorate, and impermeant anions) without discernible change in membrane potential. Caffeine-contracture tension also was augmented by diethyl ether. Caffeine-contracture tension was not enhanced by several other twitch-potentiating agents (zinc, tetraethylammonium, and piperidylmethyl androstane). Increased [Mg]0 or [Ca]0 or prior depolarization in high [K]0 did not prevent the potentiation of caffeine-contracture tension by most effective agents. However, enhancement of caffeine-contracture tension by nitrate or perchlorate was largely eliminated by both of these procedures. The monovalent impermeant anions differed from one another in the intensity of their effects on caffeine contractures, and these differences still were evident in the presence of high [K]0. These differences must be attributed to actions exerted at the external surface of the plasma membrane which encloses the fiber and lines its transverse tubules.
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Foulks et al. (1971) studied this question.
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