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1 CMRL, Simon Fraser University, Burnaby, BC, Canada; Cardiovascular Sciences, Child and Family Research Institute, Vancouver, BC, Canada
2 Cardiovascular Sciences, Child and Family Research Institute, Vancouver, BC, Canada; Anesthesiology, Pharmacology and Therapeutics, University of British Columbia, Vancouver, BC, Canada
3 Anesthesiology, Pharmacology and Therapeutics, University of British Columbia, Vancouver, BC, Canada
4 Cardiology, Hospital de Sant Pau, Barcelona, Spain
* To whom correspondence should be addressed. E-mail: tibbits{at}sfu.ca.
Store-operated Ca2+ entry (SOCE), Ca2+ entry triggered by the depletion of the intracellular Ca2+ stores, has been observed in many cell types, but only recently has it been suggested to occur in cardiomyocytes. In the present study, we demonstrate a SOCE-dependent SR Ca2+ loading, which was not altered by inhibition of L-type Ca2+ channels, reverse mode Na+-Ca2+ exchange (NCX), or non-selective cation channels. In contrast, lowering of the extracellular [Ca2+] to 0 mM, or the addition of either 0.5 mM Zn2+ or the putative store-operated channel (SOC) inhibitor SKF-96365 (100 µM) all inhibited SR Ca2+ loading at rest. Interestingly, inhibition of forward mode NCX with 30 µM KB-R7943 stimulated SOCE significantly and resulted in enhanced SR Ca2+ loading. In addition, manipulation of the extracellular and intracellular Na+ concentrations further illustrated the modulatory role of NCX in SOCE-mediated SR Ca2+ loading. While there is little knowledge about SOCE in cardiomyocytes, the present results suggest that this mechanism together with NCX may play an important role in SR Ca2+ homeostasis. The data also intimate the presence of microdomains unique to the neonatal cardiomyocyte. These findings may be of particular importance during neonate open heart surgery, in which uncontrolled SOCE could lead to SR Ca2+ overload and arrhythmogenesis.
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