Effect of sodium deprivation on contraction and charge movement in frog skeletal muscle fibres

Abstract

Measurements of isometric tension were performed in single twitch skeletal muscle fibres and the effect of extracellular Na+ removal on contraction was investigated. Na+ withdrawal brought about an increase in the amplitude of K+ contractures and their time course became faster. The potentiation of K+ contractures depended strongly on extracellular Ca2+ and developed slowly following an exponential time course with a time constant of approximately 8 min. Removal of extracellular Na+ greatly increased the amplitude of caffeine contractures and lowered its threshold: caffeine (0.5 mM) had no effect on resting tension in Ringer's but produced contractures in Na(+)-free solutions. Intramembrane charge movement (charge 1) was monitored in contracting voltage-clamped segments of frog skeletal muscle fibres using the triple-Vaseline-gap technique. Movement of charge 1 did not depend on the presence of extracellular Na+. However, the mechanical threshold decreased by approximately 10 mV at several pulse durations and the charge which produced just detectable contractions decreased by approximately 5 nC microF-1 in the absence of extracellular Na+. Intracellular heparin (40 mg ml-1) increased the mechanical threshold by approximately 20 mV without affecting the movement of charge 1. The effect of Na(+)-free solutions on the mechanical threshold was additive to that of heparin. It is concluded that the effects of Na(+)-withdrawal on contraction take place at a location beyond the voltage sensor of excitation-contraction coupling.

Ca2+ Influx via the Na+/Ca2+ Exchanger Is Enhanced in Malignant Hyperthermia Skeletal Muscle

“…This potential mechanism is supported by a number of electrophysiological studies that demonstrate that TRPCs allow permeation of Na ϩ as well as Ca 2ϩ (42,43 (44,45). The absence of muscle activation in MHN muscles is in agreement with previous studies where the effect of extracellular Na ϩ withdrawal had been studied in diverse muscle preparations (15,46,47).…”

Sodium/calcium exchange in amphibian skeletal muscle fibers and isolated transverse tubules

“…Parallel measurement of intracellular [Ca 2ϩ ] using fluo 3 as the Ca 2ϩ indicator revealed that, when the fiber was exposed to zero external [Na ϩ ], only a small increase in cytoplasmic [Ca 2ϩ ] that was partially reversed on reperfusing the fiber with Ringer was observed. This limited increase in [Ca 2ϩ ] was not enough to produce contractures, in agreement with previous reports (13,26). However, fibers became somewhat swollen when exposed to external solutions without Na ϩ .…”

“…In agreement with this rather low Ca 2ϩ affinity, to detect Na ϩ -dependent Ca 2ϩ efflux in amphibian single fibers, it is necessary to increase the intracellular Ca 2ϩ concentration ([Ca 2ϩ ]) well above its resting level (22). The reverse mode of the exchanger may cause the enhancement of contraction that takes place after external Na ϩ withdrawal in phasic (8,13,17,26) or tonic (24) amphibian skeletal muscle fibers.…”

Long-term depolarization regulates the α 1s subunit of skeletal muscle Ca 2+ channels and the amplitude of L-type Ca 2+ currents

“…In fact, although our depolarizing solutions contained a low concentration of sodium ions and therefore a decreased efflux of Ca 2+ through the Na + /Ca 2+ exchanger might be expected, the exchanger appears to play a minor role in this process as compared to its role in cardiac muscle and tonic fibers [5]. Furthermore, charge movement is not affected by deprivation of extracellular sodium ions [16]. Finally, we did not observe changes in fluorescence that might indicate an elevation in resting myoplasmic Ca 2+ by protracted depolarization.…”