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Assessment of Myofilament Ca2+ Sensitivity Underlying Cardiac Excitation-contraction Coupling
Published on: August 1, 2016
Cardiac sodium transport and excitation-contraction coupling
J M Aronsen1, F Swift, O M Sejersted
1Institute for Experimental Medical Research, Oslo University Hospital Ullevål and University of Oslo, Oslo, Norway.
Journal of Molecular and Cellular Cardiology
|June 19, 2013
Summary
Sodium ions (Na+) critically regulate heart muscle contraction by influencing calcium handling in specialized cellular nanodomains. Understanding these Na+ dynamics is key to cardiac excitation-contraction coupling.
Area of Science:
- Cardiovascular Physiology
- Cellular Electrophysiology
- Molecular Cardiology
Background:
- Excitation-contraction coupling (EC-coupling) in cardiomyocytes links electrical activity to muscle contraction.
- Calcium ions (Ca2+) play a central role, triggering release from the sarcoplasmic reticulum (SR) via ryanodine receptors (RyRs) and subsequent removal by SERCA2 and the Na,Ca-exchanger (NCX).
- The Na,Ca-exchanger (NCX) links cardiac Ca2+ and Na+ transport, suggesting Na+ influences EC-coupling, though mechanisms remain debated.
Purpose of the Study:
- To review current understanding of Na+-mediated regulation of cardiac EC-coupling.
- To focus on the role of subcellular microdomains and Na+ transport proteins.
- To explore the impact of Na+ on Ca2+ handling and cardiomyocyte contraction.
Main Methods:
- Literature review of existing data and concepts.
- Analysis of theoretical models and experimental evidence concerning Na+ compartmentalization.
- Focus on the interplay between Na+ channels, NCX, and Na,K-ATPase (NKA) in nanodomains.
Main Results:
- Na+ accumulation in specific subcellular nanodomains, rather than bulk cytosol, may trigger reverse mode NCX, influencing Ca2+ influx during action potentials.
- The Na,K-pump (NKA) can create local Na+ depletion in other nanodomains.
- Na+ levels regulate the balance between SERCA2 and NCX, affecting cytosolic Ca2+ removal and SR Ca2+ load during Ca2+ transient decay.
Conclusions:
- Voltage-gated Na+ channels, NCX, and the NKA α2-isoform likely regulate cardiac EC-coupling by controlling Na+ concentration within specific subcellular nanodomains.
- Subcellular Na+ gradients and nanodomain dynamics are crucial for precise control of cardiomyocyte contraction.
- Further research is needed to fully elucidate the precise nature and function of these Na+ nanodomains.
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