Abstract
The time course of K contractures can be significantly prolonged in the frogs, Rana pipiens and Leptodactylus insularis by low concentrations of caffeine. This effect of caffeine is not due to impairment of the fiber relaxing system. Under conditions where contractile repriming is delayed (low temperature) an extra amount of activator can be released by caffeine, in addition to that released by K. The source of this extra amount of activator is intracellular since its release can be shown in a 0% Ca EGTA [ethylene bis(oxyethylenenitrilo)tetraacetic acid] medium. Local anesthetics, tetracaine and to a lesser extent procaine affect the release of contractile activator, without impairing the contractile machinery itself. The time course of K contracture may be controlled by a membrane mechanism which is activated upon depolarization and later inactivates with time. The effect of caffeine and local anesthetics can be explained by assuming that the former prolongs the inactivation time course while the latter shortens it.