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This Article Full Text Full Text (PDF) Supplemental Figures and Tables All Versions of this Article: 290/6/C1572    most recent 00226.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Huang, J. Articles by Tibbits, G. F. Search for Related Content PubMed PubMed Citation Articles by Huang, J. Articles by Tibbits, G. F.

MEMBRANE TRANSPORTERS, ION CHANNELS, AND PUMPS

Store-operated Ca²⁺ entry modulates sarcoplasmic reticulum Ca²⁺ loading in neonatal rabbit cardiac ventricular myocytes

¹Cardiac Membrane Research Laboratory, Simon Fraser University, Burnaby; ²Cardiovascular Sciences, Child and Family Research Institute, Vancouver; ³Department of Anesthesiology, Pharmacology and Therapeutics, University of British Columbia, Vancouver, British Columbia, Canada; and ⁴Laboratorio de Fisiología Celular, Cardiología, Hospital de Sant Pau, Barcelona, Spain

Submitted 11 May 2005 ; accepted in final form 5 January 2006

Store-operated Ca²⁺ entry (SOCE), which is Ca²⁺ entry triggered by the depletion of 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 have demonstrated SOCE-dependent sarcoplasmic reticulum (SR) Ca²⁺ loading (load_SR) that was not altered by inhibition of L-type Ca²⁺ channels, reverse mode Na⁺/Ca²⁺ exchange (NCX), or nonselective cation channels. In contrast, lowering the extracellular [Ca²⁺] to 0 mM or adding either 0.5 mM Zn²⁺ or the putative store-operated channel (SOC) inhibitor SKF-96365 (100 µM) inhibited load_SR at rest. Interestingly, inhibition of forward mode NCX with 30 µM KB-R7943 stimulated SOCE significantly and resulted in enhanced load_SR. In addition, manipulation of the extracellular and intracellular Na⁺ concentrations further demonstrated the modulatory role of NCX in SOCE-mediated SR Ca²⁺ loading. Although there is little knowledge of SOCE in cardiomyocytes, the present results suggest that this mechanism, together with NCX, may play an important role in SR Ca²⁺ homeostasis. The data reported herein also imply the presence of microdomains unique to the neonatal cardiomyocyte. These findings may be of particular importance during open heart surgery in neonates, in which uncontrolled SOCE could lead to SR Ca²⁺ overload and arrhythmogenesis.

cardiac ontogeny; cardiac excitation-contraction coupling; calcium homeostasis

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