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Cardiovascular Research 1995 30(2):212-221; doi:10.1016/S0008-6363(95)00020-8
© 1995 by European Society of Cardiology
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Copyright © 1995, European Society of Cardiology

Intracellular calcium transients underlying interval-force relationship in whole rat hearts: effects of calcium antagonists

Christian E. Zaugg*,a, Shoji Kojimaa, Shao T. Wua, Joan Wikman-Coffelta, William W. Parmleya and Peter T. Buserb

aDepartment of Medicine and Cardiovascular Research Institute, University of California San Francisco, San Francisco, CA 94143, USA
bDivision of Cardiology, Department of Medicine, University Hospitals, Basel, Switzerland

* Corresponding author. M-1186, Cardiology Division, University of California San Francisco, 505 Parnassus, San Francisco, CA 94143-0124, USA. Tel.: 415-476-1710; Fax 415-476-0424.

Objectives: Much of the understanding about the cardiac interval-force relationship of the whole heart, including mechanical restitution and postextrasystolic potentiation (PESP), has been inferred from isolated muscle studies. We tested whether results from isolated muscles about intracellular Ca2+([Ca2+]i) transients underlying the interval-force relationship can be substantiated in whole hearts. Additionally, we investigated whether Ca2+ antagonists could alter [Ca2+]i transients underlying mechanical restitution and postextrasystolic potentiation. Methods: [Ca2+]i transients were studied in isolated perfused rat hearts by surface fluorometry and Indo-1. Using computer-controlled pacing protocols, we performed restitution curves for left ventricular developed pressure and [Ca2+]i (developed pressure and [Ca2+]i plotted as a function of extrasystolic intervals). To quantify restitution curves, we fitted monoexponential functions to plots and analyzed their shift and slope. Then, we used Ca2+ antagonists, low extracellular Ca2+([Ca2+]o) and PESP to modify restitution curves. [Ca2+]i transients in isolated rat hearts were interpreted as Ca2+ released from the sarcoplasmic reticulum. Results: Interval-dependent changes in developed pressure were strongly correlated to interval-dependent changes in the amplitude of [Ca2+]i transients in isolated whole rat hearts. Additionally, nifedipine and low [Ca2+]o led to similar downward shifts but not to a changed slope of restitution curves for [Ca2+]i. On the other hand, PESP increased the slope of restitution curves for [Ca2+]i. Furthermore, the effect of PESP on developed pressure was blunted by high concentrations of Ca2+ antagonists. Conclusions: The results from isolated muscles about [Ca2+]i transients underlying the interval-force relationship could be substantiated in whole hearts. Additionally, low [Ca2+]i (induced by nifedipine or low [Ca2+]o) decreased the maximal Ca2+ release of the sarcoplasmic reticulum but did not change the release kinetics. On the other hand, PESP presumably accelerated Ca2+ release kinetics of the sarcoplasmic reticulum.

KEYWORDS Interval-force relationship; Postextrasystolic potentiation; Calcium intracellular concentration; Calcium antagonists; Indo-1; Surface fluorometry; Rat heart; Calcium transients


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