Abstract
The inactivation of potassium (K) contractures induced by prolonged conditioning depolarization and repriming after 190 mM K+ contractures were studied at both room and low temperatures using frog single twitch muscle fibers. Effects of conditioning K+ depolarization and external Ca2+ reduction on the biphasic K contractures were also studied. When the conditioning depolarization with 15-30 mM K+ was prolonged, the peak tension of test 190 mM K+ contractures was inhibited in parallel with the shortening of plateau duration at both room and low temperatures. Such parallel changes were also observed during the early stage of repriming after 190 mM K+ contracture at both temperatures. On the other hand, the peak tension of the secondary component of the test 80 mM K+ contractures was rather potentiated by the conditioning depolarization, even though the time course of the component was markedly shortened. The foregoing changes were also illustrated in a diagramatic way. These results suggested that the peak tension and the time course of the test K contractures after conditioning depolarization and during repriming may be determined by a balance between the activation and the inactivation processes of the contractures. This view is supported by the results obtained under conditions in which the concentration of external Ca2+ was reduced. Furthermore, based on additional experimental results, it was suggested that the initial component is not accompanied by an inactivation process and that Ca uptake by sarcoplasmic reticulum may partially contribute to determining the spontaneous relaxation phase of the secondary component, at least at room temperature.
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