CHARACTERISTICS OF CALCIUM DEPENDENT REPOLARIZATION OF MUSCLE ACTION POTENTIAL PROLONGED BY ZINC IONS

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Ca^<2+> removal from Ringer's solution containing Zn^<2+> prolongs the action potential of frog skeletal muscle. In order to clarify the mechanism of this phenomenon, the action potentials were recorded in three different conditions: transverse tubule-disrupted (detubulated) fibers in Ringer's solution with Zn^<2+>, intact fibers in Ringer's with tetraethylammonium (TEA), and intact fibers in Ringer's with Zn^<2+> in the presence of Ca^<2+> antagonists. In detubulated fibers Ca^<2+> removal elongated the deration of the action potential but did not alter the maximum rate of fall in the presence of Zn^<2+> (50μM). TEA (30mM) in the medium slowed the repolarization of the action potentials in intact fibers. Ca^<2+> did not give any effect on the action potential in this solution. Both diltiazem (10μM) and (L) (-)-verapmil (10μM) did not alter the parameters of the action potential in the presence of Zn^<2+> (50μM). These results indicate that the objective phenomenon rises from the nature of both surface and tubular membranes, concerns with Ca^<2+>-dependent K^+ channels and is independent of Ca^<2+> channels. This leads to the hypothesis that small fraction of membrane-bound Ca^<2+> is released by membrane depolarization, causing activation of Ca^<2+>-dependent K^+ channels.
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