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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.
Insights
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.
Abstract:
Physiologically, human atrial and ventricular myocardium are coupled by an identical beating rate and rhythm. However, contractile behavior in atrial myocardium may be different from that in ventricular myocardium, and little is known about intracellular Ca(2+) handling in human atrium under physiological conditions. We used rapid cooling contractures (RCCs) to assess sarcoplasmic reticulum (SR) Ca(2+) content and the photoprotein aequorin to assess intracellular Ca(2+) transients in atrial and ventricular muscle strips isolated from nonfailing human hearts. In atrial myocardium (n = 19), isometric twitch force frequency dependently (0. 25-3 Hz) increased by 78 +/- 25% (at 3 Hz; P < 0.05). In parallel, aequorin light signals increased by 111 +/- 57% (P < 0.05) and RCC amplitudes by 49 +/- 13% (P < 0.05). Similar results were obtained in ventricular myocardium (n = 13). SR Ca(2+) uptake (relative to Na(+)/Ca(2+) exchange) frequency dependently increased in atrial and ventricular myocardium (P < 0.05). With increasing rest intervals (1-240 s), atrial myocardium (n = 7) exhibited a parallel decrease in postrest twitch force (at 240 s by 68 +/- 5%, P < 0.05) and RCCs (by 49 +/- 10%, P < 0.05). In contrast, postrest twitch force and RCCs significantly increased in ventricular myocardium (n = 6). We conclude that in human atrial and ventricular myocardium the positive force-frequency relation results from increased SR Ca(2+) turnover. In contrast, rest intervals in atrial myocardium are associated with depressed contractility and intracellular Ca(2+) handling, which may be due to rest-dependent SR Ca(2+) loss (Ca(2+) leak) and subsequent Ca(2+) extrusion via Na(+)/Ca(2+) exchange. Therefore, the influence of rate and rhythm on mechanical performance is not uniform in atrial and ventricular myocardium.