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Assessment of Myofilament Ca2+ Sensitivity Underlying Cardiac Excitation-contraction Coupling
Published on: August 1, 2016
Calcium and Excitation-Contraction Coupling in the Heart
David A Eisner1, Jessica L Caldwell2, Kornél Kistamás2
1From the Unit of Cardiac Physiology, Division of Cardiovascular Sciences, Manchester Academic Health Sciences Centre, University of Manchester, United Kingdom. eisner@manchester.ac.uk.
Insights
Cardiac contractility relies on precise intracellular calcium ([Ca2+]) regulation. This review details how calcium-induced calcium release and coupled transporters ensure sufficient systolic calcium for contraction and low diastolic calcium for relaxation.
Area of Science:
- Cardiology
- Molecular Biology
- Cell Physiology
Background:
- Cardiac contractility is modulated by intracellular calcium concentration ([Ca2+]i).
- Optimal cardiac function necessitates high systolic and low diastolic [Ca2+]i.
- Calcium-induced calcium release from the sarcoplasmic reticulum is a primary source of contraction-triggering calcium.
Purpose of the Study:
- To review the regulation of calcium release initiation and termination in cardiac cells.
- To explore the structural and functional coupling mechanisms governing intracellular calcium cycling.
- To discuss factors influencing diastolic calcium levels and overall calcium signaling.
Main Methods:
- Review of existing literature on cardiac calcium handling.
- Analysis of the structural organization of calcium transporters within dyads.
- Examination of the balance between calcium influx and efflux across cellular membranes.
Main Results:
- Structural coupling within dyads ensures proximity of calcium entry to release sites.
- Functional coupling requires a balance of calcium fluxes for steady-state conditions.
- Factors like calcium buffers, mitochondria, and calcium leak critically influence diastolic calcium regulation.
Conclusions:
- Precise control of intracellular calcium cycling is essential for normal cardiac function.
- Both structural and functional coupling mechanisms are vital for fine-tuning calcium release.
- Understanding these regulatory aspects provides insight into cardiac health and disease.
Abstract:
Cardiac contractility is regulated by changes in intracellular Ca concentration ([Ca2+]i). Normal function requires that [Ca2+]i be sufficiently high in systole and low in diastole. Much of the Ca needed for contraction comes from the sarcoplasmic reticulum and is released by the process of calcium-induced calcium release. The factors that regulate and fine-tune the initiation and termination of release are reviewed. The precise control of intracellular Ca cycling depends on the relationships between the various channels and pumps that are involved. We consider 2 aspects: (1) structural coupling: the transporters are organized within the dyad, linking the transverse tubule and sarcoplasmic reticulum and ensuring close proximity of Ca entry to sites of release. (2) Functional coupling: where the fluxes across all membranes must be balanced such that, in the steady state, Ca influx equals Ca efflux on every beat. The remainder of the review considers specific aspects of Ca signaling, including the role of Ca buffers, mitochondria, Ca leak, and regulation of diastolic [Ca2+]i.
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