期刊
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY
卷 284, 期 4, 页码 C826-C838出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpcell.00465.2002
关键词
calcium; lipid metabolites; excitation-contraction coupling; heart
资金
- NHLBI NIH HHS [R01HL-62226] Funding Source: Medline
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 (I-Ca,I-L) and outward currents. LPlasC-induced alterations in contraction and I-Ca,I-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.
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