Ryanodine receptors: waking up from refractoriness
Abstract
This editorial refers to ‘Recovery of cardiac calcium release is controlled by sarcoplasmic reticulum refilling and ryanodine receptor sensitivity’ by H.R. Ramay et al., pp. 598–605, this issue. Ca2+-induced Ca2+ release (CICR) from the sarcoplasmic reticulum (SR) via ryanodine receptors (RyRs) ultimately governs cardiac muscle force and can be considered as an amplification system for cardiac Ca2+ signals. CICR is initiated by Ca2+ influx via voltage-dependent L-type Ca2+ channels.1 Unlike skeletal muscle fibres, each cardiac myocyte can produce an amount of force (and a Ca2+ transient) that is graded by the amplitude of the Ca2+ current. How this works had remained a mystery for years because CICR is a positive feedback mechanism and one would expect, and mathematically predict, an all-or-none behaviour for these Ca2+ signals.2 As it turns out, regulation of the amplitude of the cardiac Ca2+ transients is implemented by virtue of a local control process, recruiting fewer or more Ca2+ sparks as needed to generate a small or large Ca2+ transient. Ca2+ sparks are subcellular elementary SR Ca2+ release signals, each of which is an all-or-none CICR event by itself, consistent with the predictions for a positive feedback system. Since the discovery of Ca2+ sparks, the combined efforts of many research groups have particularized features of their activation. However, much less is known about the mechanism(s) restraining CICR and leading to Ca2+ spark termination. In an elegant…
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