Sodium-calcium exchange in transverse tubules isolated from frog skeletal muscle

Donoso, P; Hidalgo, Cecilia

doi:10.1016/0005-2736(89)90491-4

Cited by 32 publications

(22 citation statements)

References 27 publications

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“…Na ϩ -dependent Ca 2ϩ fluxes have been reported in amphibian skeletal muscle (9,10), and human myotubes (7). NCX has been observed in sarcolemmal fractions isolated from mammalian muscles (11) and in t-tubules isolated from amphibian muscles (12,13). In addition, the reverse mode of the exchanger seems to mediate the enhancement of contraction that takes place after external Na ϩ withdrawal in phasic and tonic amphibian skeletal muscle fibers (14 -17).…”

Section: Malignant Hyperthermia (Mh) Ismentioning

confidence: 99%

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

Altamirano

Eltit

Robin

et al. 2014

Journal of Biological Chemistry

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Section: Malignant Hyperthermia (Mh) Ismentioning

confidence: 99%

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

Altamirano

Eltit

Robin

et al. 2014

Journal of Biological Chemistry

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“…Since the differential action of ryanodine on muscle SR is largely dependent on the ionic environment (Meissner 1986), some alteration of the ionic composition in the intertriadic space, as a consequence of the external Na+ replacement by choline, could favour the increase in open probability of channels rather than the decrease in conductance. In this regard, the Na+/Ca2+ exchanger, whose existence has been recently demonstrated in transverse tubules from frog skeletal muscle (Donoso and Hidalgo 1989), could be of some relevance.…”

Section: Discussionmentioning

confidence: 98%

The correlation between the increase in slow outward current and in contraction induced by caffeine, ryanodine, and rapid cooling in voltage-clamped frog muscle fibers

Nasri-Sebdani

Traoré²,

Mouzou³

et al. 1991

Can. J. Physiol. Pharmacol.

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The effects of caffeine, ryanodine, and rapid cooling were tested on the depolarization-induced contraction and the apamin-insensitive slow outward current (Iso) of voltage-clamped (double mannitol gap) single frog muscle fibers. Subthreshold caffeine concentrations (0.5-2 mM) induced a monotonic increase in contractile and Iso amplitude. Whatever the concentration, the increase in contraction was roughly twice the one in current. Similar results were obtained upon rapid cooling (20-4 degrees C) in the presence of 0.5 mM caffeine. In the absence of external Na+ (choline-substituted) 10(-5) M ryanodine induced a delayed increase (approximately 30 min) in contraction and in current, shortly before the development of a drastic and irreversible contracture. Here again, the increase in contraction was twice that in current. In the presence of 5 mM tetraethylammonium (TEA) and (or) 25 nM charybdotoxin, 2 mM caffeine still induced a strong facilitating effect on contraction but the parallel increase in current was strongly reduced. The linear relationship between the increase in current and contractile amplitude has a slope approximately 0.5 (whatever the drug used to increase contractility); it is approximately 0.1 in the presence of TEA and (or) charybdotoxin. In conclusion, provided the changes in contractile amplitude are caused by parallel changes in depolarization-induced sarcoplasmic reticulum Ca2+ release, about 50% of the apamin-insensitive Iso is controlled by internal Ca2+ release. The main part of this current corresponds to the TEA- and charybdotoxin-sensitive component of Iso.

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“…The Na + -Ca 2+ exchanger operates electrogenically [7] and may produce a change in the membrane potential.…”

Section: Effects Of Low Na + -Solution On Membrane Potentialmentioning

confidence: 99%

Na + -Ca 2+ exchange induces low Na + contracture in frog skeletal muscle fibers after partial inhibition of sarcoplasmic reticulum Ca 2+ -ATPase

Même¹,

Léoty²

1999

Pfl�gers Archiv European Journal of Physiology

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Contractile responses due to reduction in external sodium concentration ([Na+]o) were investigated in twitch skeletal muscle fibers of frog semitendinosus. Experiments were conducted after partial inhibition of sarcoplasmic reticulum Ca(2+)-ATPase by cyclopiazonic acid (CPA). In the absence of CPA, Na+ withdrawal failed to produce any change in resting tension. In the presence of CPA (2-10 microM), [Na+]o reduction induced a transient contracture without a significant change in the resting membrane potential. The amplitude of the contracture displayed a step dependence on [Na+]o, was increased by K(+)-free medium and was prevented in Ca(2+)-free medium. This contracture was inhibited by various blockers of the Na(+)-Ca2+ exchange but was little affected by inhibitors of sarcolemmal Ca(2+)-ATPase or mitochondria. When sarcoplasmic reticulum function was impaired, low-Na+ solutions caused no contracture. These results provide evidence that skeletal muscle fibers possess a functional Na(+)-Ca2+ exchange which can mediate sufficient Ca2+ entry to activate contraction by triggering Ca2+ release from sarcoplasmic reticulum when the sodium electrochemical gradient is reduced, and sarcoplasmic reticulum Ca(2+)-ATPase is partially inhibited. This indicates that when the sarcoplasmic reticulum Ca(2+)-ATPase is working (no CPA), Ca2+ fluxes produced by the exchanger are buffered by the sarcoplasmic reticulum. Thus the Na(+)-Ca2+ exchange may be one of the factors determining sarcoplasmic reticulum Ca2+ content and thence the magnitude of the release of Ca2+ from the sarcoplasmic reticulum.

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Sodium-calcium exchange in transverse tubules isolated from frog skeletal muscle

Cited by 32 publications

References 27 publications

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

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

The correlation between the increase in slow outward current and in contraction induced by caffeine, ryanodine, and rapid cooling in voltage-clamped frog muscle fibers

Na + -Ca 2+ exchange induces low Na + contracture in frog skeletal muscle fibers after partial inhibition of sarcoplasmic reticulum Ca 2+ -ATPase

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