Abstract
1. Mouse extensor digitorum longus and soleus muscles respond to a sudden maintained increase in external K ion concentration with a fast contracture which inactivates and is followed by a slow contracture. 2. The slow contracture could not be selectively eliminated by altering the tonicity, ionic strength, anionic composition or buffer system of the external solution and depended only on the increase on external potassium concentration. The slow contracture differed from the fast K contracture in its time course, temperature sensitivity, fibre type dependence, and inactivation kinetics. The fast and slow contractures were similarly altered by changes in external anion species, by changes in external divalent cations, and by the presence of 20 mM-caffeine. 3. The mechanism and functional significance of the slow contracture are obscure. The results suggest that its generation is not identical to that of the fast contracture, but may depend, in part, upon the normal activation processes.
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