To determine if an Ag(+)-induced
contracture is associated with the Ca(2+)-induced Ca2+ release mechanism in the sarcoplasmic reticulum, effects of Ca(2+)-induced Ca2+ release modulators on the Ag(+)-induced
contracture were studied with single fibers of frog toe skeletal muscle. The fiber treated with 1 mM
caffeine contracted significantly much more than controls without
caffeine at Ag+ concentrations below 1 microM.
Procaine shifted the Ag+ concentration-tension curve to the right, dose-dependently. When 10 mM
procaine was applied to contracting fibers not treated with
caffeine, the duration of 5 microM Ag(+)-induced
contracture was shortened with a little decrease in tension amplitude, that was different from the effect of
procaine on
caffeine contracture. In
caffeine solution, 0.5 microM Ag+ caused a long-lasting
contracture with sometimes two peaks. 2 mM
procaine led to disappearance of such two peaks, resulting in shortening of the
contracture. K+
contracture was potentiated by 1 mM
caffeine only at lower concentrations of K+, and inhibited by 10 mM
procaine. These results suggest that the Ag(+)-induced
contracture is composed of two components: Ca(2+)-induced Ca2+ release-dependent and -independent. 5 microM Ag(+)-induced
contracture slowly relaxed with a wavy tension pattern to the resting level when 0.05 mM
dithiothreitol was applied around peak of the tension. This relaxation was accelerated by
procaine application. These findings may be explained by attributing a portion of Ag(+)-induced
contracture to the effect of Ca2+ released through the Ca(2+)-induced Ca2+ release mechanism in the sarcoplasmic reticulum.