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Am J Physiol Cell Physiol 284: C826-C838, 2003. First published November 27, 2002; doi:10.1152/ajpcell.00465.2002
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Vol. 284, Issue 4, C826-C838, April 2003

Alterations in Ca2+ cycling by lysoplasmenylcholine in adult rabbit ventricular myocytes

Shi J. Liu1, Richard H. Kennedy1, Michael H. Creer2, and Jane McHowat2

1 Departments of Pharmaceutical Sciences and Pharmacology and Toxicology, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205; and 2 Department of Pathology, St. Louis University Medical School, St. Louis, Missouri 63104

We previously reported that lysoplasmenylcholine (LPlasC) altered the action potential (AP) and induced afterdepolarizations in rabbit ventricular myocytes. In this study, we investigated how LPlasC alters excitation-contraction coupling using edge-motion detection, fura-PE3 fluorescent indicator, and perforated and whole cell patch-clamp techniques. LPlasC increased contraction, myofilament Ca2+ sensitivity, systolic and diastolic free Ca2+ levels, and the magnitude of Ca2+ transients concomitant with increases in the maximum rates of shortening and relaxation of contraction and the rising and declining phases of Ca2+ transients. In some cells, LPlasC induced arrhythmias in a pattern consistent with early and delayed aftercontractions. LPlasC also augmented the caffeine-induced Ca2+ transient with a reduction in the decay rate. Furthermore, LPlasC enhanced L-type Ca2+ channel current (ICa,L) and outward currents. LPlasC-induced alterations in contraction and ICa,L were paralleled by its effect on the AP. Thus these results suggest that LPlasC elicits distinct, potent positive inotropic, lusitropic, and arrhythmogenic effects, resulting from increases in Ca2+ influx, Ca2+ sensitivity, sarcoplasmic reticular (SR) Ca2+ release and uptake, SR Ca2+ content, and probably reduction in sarcolemmal Na+/Ca2+ exchange.

calcium; lipid metabolites; excitation-contraction coupling; heart


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