The purpose of this investigation was to explore the possible mechanism of muscle contracture and twitch depression induced by arsenite in the mouse diaphragm. Arsenite-contracture was dependent on extracellular Ca2+ both EGTA and Ca2+-channel blockers (nifedipine and verapamil) inhibited arsenite-contracture. However, the activators caffeine and ryanodine and the inhibitor ruthenium red of the Ca2+ releasing channel of sarcoplasmic reticulum (SR) all exerted a profound inhibitory action on arsenite-contracture. Neither the Ca2+-release nor the Ca2+-ATPase activity of S.R. were affected by 50 arsenite. These findings indicate a possibility that arsenite induced muscle contracture by enhancing Ca2+-entry which further induced Ca2+-release from S.R. Moreover, the possible mechanism of twitch blockade induced by arsenite was studied by an electrophysiological technique. The frequency of miniature endplate potential (m.e.p.p.) was initially increased but eventually aboUshed by arsenite, while the amplitude of m.e.p.p. remained unaffected and that of endplate potential rapidly declined. It is considered that arsenite increased the spontaneous release of transmitter by enhancing Ca2+ entry into the nerve terminal and inhibited the evoked transmitter release possibly by acting at a certain site which governs transmitter release.
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