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Ca(2+) handling in isolated human atrial myocardium
L S Maier1, P Barckhausen, J Weisser
1Abteilung Kardiologie und Pneumologie, Zentrum Innere Medizin, Georg-August-Universität Göttingen, 37075 Göttingen, Germany.
American Journal of Physiology. Heart and Circulatory Physiology
|September 20, 2000
Summary
Human atrial and ventricular muscle show similar responses to increased heart rate, but prolonged rest impairs atrial contractility due to calcium handling differences. This impacts cardiac mechanical performance.
Area of Science:
- Cardiology
- Physiology
- Molecular Biology
Background:
- Human atrial and ventricular myocardium share identical beating rates but may differ in contractile behavior.
- Intracellular calcium (Ca2+) handling in human atrium under physiological conditions is not well understood.
Purpose of the Study:
- To investigate and compare intracellular Ca2+ handling and contractile behavior in human atrial and ventricular myocardium.
- To elucidate the mechanisms underlying the force-frequency relationship and rest-interval effects in both cardiac chambers.
Main Methods:
- Utilized rapid cooling contractures (RCCs) to measure sarcoplasmic reticulum (SR) Ca2+ content.
- Employed the photoprotein aequorin to assess intracellular Ca2+ transients.
- Studied atrial and ventricular muscle strips isolated from nonfailing human hearts.
Main Results:
- Both atrial and ventricular myocardium demonstrated a positive force-frequency relation, with increased SR Ca2+ turnover.
- Atrial myocardium showed decreased postrest twitch force and RCCs with longer rest intervals, unlike ventricular myocardium.
- Rest intervals in atria may lead to SR Ca2+ loss (leak) and subsequent Ca2+ extrusion via Na+/Ca2+ exchange.
Conclusions:
- The positive force-frequency relation in human atria and ventricles is driven by enhanced SR Ca2+ turnover.
- Atrial contractility and Ca2+ handling are depressed after rest periods, suggesting rest-dependent SR Ca2+ leak.
- Rate and rhythm influence mechanical performance differently in atrial and ventricular myocardium.