The ryanodine receptors (RyRs) are a family of Ca2+ release channels found on intracellular Ca2+ storage/release organelles. The RyR channels are ubiquitously expressed in many types of cells and participate in a variety of important Ca2+ signaling phenomena (neurotransmission, secretion, etc.). In striated muscle, the RyR channels represent the primary pathway for Ca2+ release during the excitation-contraction coupling process. In general, the signals that activate the RyR channels are known (e.g., sarcolemmal Ca2+ influx or depolarization), but the specific mechanisms involved are still being debated. The signals that modulate and/or turn off the RyR channels remain ambiguous and the mechanisms involved unclear. Over the last decade, studies of RyR-mediated Ca2+ release have taken many forms and have steadily advanced our knowledge. This robust field, however, is not without controversial ideas and contradictory results. Controversies surrounding the complex Ca2+ regulation of single RyR channels receive particular attention here. In addition, a large body of information is synthesized into a focused perspective of single RyR channel function. The present status of the single RyR channel field and its likely future directions are also discussed.

https://www.physiology.org/doi/pdf/10.1152/physrev.00013.2002

Ryanodine Receptor Calcium Release Channels

Voltage sensor of excitation-contraction coupling in skeletal muscle.

The role of Ca2+ ions in excitation-contraction coupling of skeletal muscle fibres.

1. The effect of caffeine on the initiation of isometric tension in isolated twitch muscle fibres of the frog was recorded with a mechano-electrical transducer.

2. In Ringer solution as well as in solutions containing 95 m M-K2SO4, caffeine (6-10 m M) caused reversible contractures. Tension of maximal potassium contractures was reached with a half-time of 2-4 sec.

3. Caffeine caused a shift to lower potassium concentrations of the S-shaped curve which relates peak tension to log. [K]o or membrane potential. In subthreshold concentrations of caffeine (1·5 m M) the potassium concentration at which half of maximal tension was reached shifted from 30 to 16 m M-K (-39 to -53 mV).

4. In the ‘steady state’ the ability of fibres to develop tension is related to log. [K]o or membrane potential by an S-shaped curve whose half value shifted from 28 to 45 m M-K (-41 to -29 mV) when 1·5 m M caffeine was applied.

5. Fibres were most sensitive to caffeine at membrane potentials between -50 and -20 mV.

6. The mechanical activity caused by caffeine was ‘stabilized’ by an increase in [Ca]o or [Mg]o resembling the stabilizing action of these ions on potassium contractures or on the sodium permeability of excitable membranes.

7. Tetracaine in low concentrations (0·04-0·1 m M) increased the threshold for mechanical activation and shortened the plateau of potassium contractures. Higher concentrations (1-2 m M) suppressed mechanical activity completely.

8. Tetracaine, 0·04 m M, was sufficient to suppress tension caused by a 100 times stronger concentration of caffeine. With higher concentrations of caffeine the inhibitory action of tetracaine could be reversed.

9. Fibres which were immersed in subthreshold concentrations of caffeine either in Ringer solution or in a solution with 95 m M-K2SO4 developed a strong contracture after a sudden drop in temperature from 20 to 1-3° C.

10. The fast activation of the whole cross-section of the muscle fibre caused by caffeine and its dependence on membrane potential, tetracaine and external alkali earth ions favours the idea that the drug acts at some part of the sarcotubular system which is easily accessible for external ions and drugs and in close connextion with the surface membrane.

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.1968.sp008394

The action of caffeine on the activation of the contractile mechanism in striated muscle fibres

Skeletal muscle fatigue is defined as the fall of force or power in response to contractile activity. Both the mechanisms of fatigue and the modes used to elicit it vary tremendously. Conceptual and technological advances allow the examination of fatigue from the level of the single molecule to the intact organism. Evaluation of muscle fatigue in a wide range of disease states builds on our understanding of basic function by revealing the sources of dysfunction in response to disease.

Skeletal Muscle Fatigue

Calcium ions are considered to be necessary in reactions linking the electrical and mechanical events in muscle fibres (reviewed by Sandow, 1952). But, whereas the effect of calcium ions on excitable membranes (reviewed by Shanes, 1958) and muscle 'models' (reviewed by Hasselbach, 1962) have been fully investigated during the last ten years, less is known about how external calcium influences the process which controls the development of tension in skeletal muscle fibres. This paper aims at giving some information about the properties of this system, which is regarded as the first of several links coupling excitation and contraction. Single fibres were used to achieve a quick change of the external ion concentrations, since a delay would have impeded the analysis of the time course of the transient contractures in twitch fibres. A preliminary account of this work already has appeared (Liittgau, 1962).

The action of calcium ions on potassium contractures of single muscle fibres

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The action of calcium ions on potassium contractures of single muscle fibres