Reappraisal of the role of sodium ions in excitation-contraction coupling in frog twitch muscle.

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Tetanic and twitch tension were recorded on isolated frog twitch fibres under experimental conditions modifying the influx of sodium ions. In current clamp conditions replacing Li+ for Na+ did not modify the electrical activity but drastically decreased the plateau of tetanic tension. In voltage clamp conditions replacing Li+ for Na+ did not modify the inward currents but induced a marked decrease of the plateau of the tetanic tension for depolarizations between the activation threshold and the reversal potential of sodium current. Under veratridine treatment, during tetanic depolarization, a slow inward sodium (or lithium) current developed. This induced a parallel increase of the tetanic tension which was much more pronounced in sodium than in lithium containing solution. The twitch tension obtained during short depolarization was increased by greater than 100% during veratridine treatment with a sizeable decrease (40%) of the delay between the end of depolarization and the beginning of tension. All these results could be reproduced in calcium-free solution. Our data confirm that the entry of sodium ions (and to a lesser extent of lithium ions) is able to modulate the release of calcium from the sarcoplasmic reticulum (SR). We discuss these results in terms of a model where sodium ions entering the compartment between the tubular membrane and the SR junctional membrane carry counter charges through the SR K+ channels and help to maintain the SR Ca2+ release. This could occur in particular during a physiological tetanic contraction where the junctional compartment is probably filled with Na+ ions and depleted of K+ ions.