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Journal ArticleDOI

Effect of chloride on Ca2+ release from the sarcoplasmic reticulum of mechanically skinned skeletal muscle fibres.

Jason Coonan, +1 more
- 01 Apr 1998 - 
- Vol. 435, Iss: 5, pp 720-730
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TLDR
The effect of intracellular Cl– on Ca2+ release in mechanically skinned fibres of rat extensor digitorum longus (EDL) and toad iliofibularis muscles was examined and acute addition of 20 mM Cl– to the myoplasm caused a 40–50% reduction in Ca2+, both in toad and rat fibres.
Abstract
The effect of intracellular Cl– on Ca2+ release in mechanically skinned fibres of rat extensor digitorum longus (EDL) and toad iliofibularis muscles was examined under physiological conditions of myoplasmic [Mg2+] and [ATP] and sarcoplasmic reticulum (SR) Ca2+ loading. Both in rat and toad fibres, the presence of 20 mM Cl–in the myoplasm increased Ca2+ leakage from the SR at pCa (i.e. –log10 [Ca2+]) 6.7, but not at pCa 8. Ca2+ uptake was not significantly affected by the presence of Cl–. This Ca2+-dependent effect of Cl– on Ca2+ leakage was most likely due to a direct action on the ryanodine receptor/Ca2+ release channel, and could influence channel sensitivity and the resting [Ca2+] in muscle fibres in vivo. In contrast to this effect, acute addition of 20 mM Cl– to the myoplasm caused a 40–50% reduction in Ca2+ release in response to a low caffeine concentration both in toad and rat fibres. One possible explanation for this latter effect is that the addition of Cl– induces a potential across the SR (lumen negative) which might reduce Ca2+ release via several different mechanisms.

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Citations
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Journal ArticleDOI

Different Ca2+ releasing action of caffeine and depolarisation in skeletal muscle fibres of the rat

TL;DR: The results show that the normal E‐C coupling mechanism in mammalian skeletal muscle does not involve just enhancing Ca2‐induced Ca2+ release, and evidently requires the removal or bypassing of the inhibitory effect of Mg2+ on the Ca2- release channels.
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ER-localized bestrophin 1 activates Ca2+-dependent ion channels TMEM16A and SK4 possibly by acting as a counterion channel

TL;DR: In this article, bestrophin 1 is localized in the endoplasmic reticulum (ER), where it interacts with stromal interacting molecule 1, the ER-Ca2+ sensor.
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Effect of sarcoplasmic reticulum Ca2+ content on action potential-induced Ca2+ release in rat skeletal muscle fibres.

TL;DR: The results show that the amount of Ca2+ released by AP stimulation in rat fast‐twitch fibres normally stays virtually constant over a wide range of SR Ca2- content, in spite of the likely large change in the electrochemical gradient for Ca2+.
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Excitation-contraction coupling and fatigue mechanisms in skeletal muscle: studies with mechanically skinned fibres.

TL;DR: This review attempts to give an insight into the key aspects of excitation–contraction (E–C) coupling and fatigue in skeletal muscle, in particular summarizing the results and perspectives obtained from studies with mechanically skinned muscle fibres.
References
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Journal ArticleDOI

Kinetics of Rapid Ca2+ Release by Sarcoplasmic Reticulum. Effects of Ca2+, Mg2+, and Adenine Nucleotides

TL;DR: Ca2+, AMP-PCP (ATP), and Mg2+ appear to act at noninteracting or interacting sites of the channel, suggesting that heavy SR vesicles contain a "Ca2+ release channel" capable of conducting Ca2+ at rates comparable with those found in intact muscle.
Journal ArticleDOI

Calcium release and ionic changes in the sarcoplasmic reticulum of tetanized muscle: an electron-probe study.

TL;DR: The unchanged distribution of a permeant anion, chloride, argues against the existence of a large and sustained transSR potential during tetanus, if the chloride permeability of the in situ SR is as high as suggested by measurements on fractionated SR.
Journal ArticleDOI

Role of ryanodine receptors.

TL;DR: A hypothesis of molecular interaction in view of the plunger model of action potential-induced Ca release is discussed, suggesting that the model could be compatible with Ryr1 and Ryr3, but incompatible with Ryanodine2.
Journal ArticleDOI

Effects of intracellular pH and [Mg2+] on excitation-contraction coupling in skeletal muscle fibres of the rat.

TL;DR: Low pH does not prevent depolarization‐induced Ca2+ release in mammalian muscle, and H+ did not readily substitute for Mg2+ at its inhibitory site on the Ca2- release channel.
Journal ArticleDOI

Magnesium inhibition of ryanodine-receptor calcium channels: evidence for two independent mechanisms.

TL;DR: It is shown that Type-I inhibition is not the sole mechanism responsible for Mg2+ inhibition, as is often assumed, and the physiological implications of this finding are discussed.
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