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Vol. 286, Issue 1, 1-8, July 1998
Laboratory of Membrane Biology, Institute of Cardiovascular
Sciences, St. Boniface General Hospital Research Centre and Department
of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg,
Manitoba, Canada R2H 2A6
Previous reports have demonstrated that lysophosphatidylcholine (LPC)
increases the intracellular concentration of calcium ([Ca++]i) in the heart; however, the
mechanisms responsible for this increase are not clear. We examined the
effect of exogenous LPC on [Ca++]i in freshly
isolated cardiomyocytes from adult rats. Our results showed that LPC
elevated the [Ca++]i in a dose-dependent
(2.5-10 µM) manner. The LPC (10 µM)-induced increase in
[Ca++]i was augmented upon increasing the
concentration of extracellular Ca++ and was abolished by
the removal of Ca++ from the medium. Preincubation of
cardiomyocytes with sarcolemmal L-type Ca++ channel
blocker, verapamil, did not affect the LPC-evoked increase in
[Ca++]i significantly. On the other hand,
ouabain, a Na+-K+ ATPase inhibitor, and low
concentrations of extracellular Na+ enhanced the LPC
response. The LPC-induced increase in [Ca++]i
was attenuated significantly by the inhibitors of
Na+-Ca++ exchanger such as Ni++ and
amiloride. Depletion of the sarcoplasmic reticulum (SR)
Ca++ stores by low micromolar concentrations of ryanodine
(a SR Ca++-release channel activator) or by thapsigargin (a
SR Ca++-pump ATPase inhibitor) depressed the LPC-mediated
increase in [Ca++]i. Combined blockade of
Na+-Ca++ exchanger and inhibition of SR
Ca++-pump or ryanodine receptor had an additive effect on
the LPC response. These observations suggest that the increase in
[Ca++]i induced by LPC depends on both
Ca++-influx from the extracellular space and
Ca++-release from the SR stores. Furthermore,
Na+-Ca++ exchange plays a critical role in the
LPC-mediated entry of Ca++ into cardiomyocytes.
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