Extract

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.

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