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Tonic component of myocardial contraction
Bohdan Lewartowski1, Urszula Mackiewicz
1Department of Clinical Physiology, Medical Centre of Postgraduate Education, Marymoncka St 99, 01-813 Warsaw, Poland. blew@cmkp.edu.pl
Cell Calcium
|April 28, 2004
Summary
Cardiac myocyte contractions involve a tonic component (TC) regulated by calcium. This review explores TC activation, primarily via sarcoplasmic reticulum calcium release, with varying mechanisms across species and heart conditions.
Area of Science:
- Cardiology
- Cell Physiology
- Biophysics
Background:
- Cardiac myocyte contractions exhibit phasic and tonic components.
- The tonic component (TC) relaxes upon repolarization, unlike the spontaneously relaxing phasic component.
Purpose of the Study:
- To review experimental data on the mechanisms activating and maintaining the tonic component of calcium transients in cardiac myocytes.
- To elucidate the physiological role and unresolved questions surrounding TC in cardiac function.
Main Methods:
- Review of existing experimental data and literature on cardiac myocyte calcium handling.
- Analysis of studies investigating calcium sources and signaling pathways involved in TC.
Main Results:
- Most Ca(2+) activating TC is released from the sarcoplasmic reticulum (SR) via ryanodine receptors (RyRs), likely activated by sustained Ca(2+) influx.
- Mechanisms differ by species: rat TC involves sustained Ca(2+) current, while guinea-pig TC is unaffected by Ca(2+) current blockers.
- In failing human hearts, TC is primarily activated by reverse mode Na(+)/Ca(2+) exchange, with negligible SR contribution.
Conclusions:
- The precise route of Ca(2+) influx activating RyRs for TC varies.
- The mechanism of TC in normal human cardiomyocytes remains uninvestigated.
- Despite extensive study, the activation, maintenance, and physiological significance of TC are not fully understood.