POSSIBLE INVOLVEMENT OF CA2-INDUCED CA2+ RELEASE MECHANISM IN AG+-INDUCED CONTRACTURE IN FROG SKELETAL-MUSCLE()

To determine if an Ag+-induced contracture is associated with the Ca2-induced Ca2+ release mechanism in the sarcoplasmic reticulum, effects of Ca2+-induced Ca2+ release modulators on the Ag+-induced contractur e were studied with single fibers of frog toe skeletal muscle. The fib er treated with 1 mM caffeine contracted significantly much more than controls without caffeine at Ag+ concentrations below 1 mu M. Procaine shifted the Ag+ concentration-tension curve to the right, dose-depend ently. When 10 mM procaine was applied to contracting fibers not treat ed with caffeine, the duration of 5 mu M Ag+-induced contracture was s hortened with a little decrease in tension amplitude, that was differe nt from the effect of procaine on caffeine contracture. In caffeine so lution, 0.5 mu M Ag+ caused a long-lasting contracture with sometimes two peaks. 2 mM procaine led to disappearance of such two peaks, resul ting in shortening of the contracture. K+ contracture was potentiated by 1 mM caffeine only at lower concentrations of K+ and inhibited by 1 0 mM procaine. These results suggest that the Ag+-induced contracture is composed of two components: Ca2+-induced Ca2+ release-dependent and -independent. 5 mu M Ag+-induced contracture slowly relaxed with a wa vy tension pattern to the resting level when 0.05 mM dithiothreitol wa s applied around peak of the tension. This relaxation was accelerated by procaine application. These findings may be explained by attributin g a portion of Ag+-induced contracture to the effect of Ca2+ released through the Ca2+-induced Ca2+ release mechanism in the sarcoplasmic re ticulum.