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Am J Physiol Cell Physiol 285: C1420-C1428, 2003; doi:10.1152/ajpcell.00534.2002
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CELLULAR METABOLISM

Calcium homeostasis in rat cardiomyocytes during chronic hypoxia: a time course study

Jian-Ming Pei,* Gennadi M. Kravtsov,* Song Wu, Rapti Das, Man Lung Fung, and Tak Ming Wong

Department of Physiology, University of Hong Kong, Hong Kong, China

Submitted 18 November 2002 ; accepted in final form 29 July 2003

The present study determined Ca2+ handling in the hearts of rats subjected to chronic hypoxia (CH). Spectrofluorometry was used to measure intracellular Ca2+ concentration ([Ca2+]i) and its responses to electrical stimulation, caffeine, and isoproterenol in myocytes from the right ventricle of rats breathing 10% oxygen for 1, 3, 7, 14, 21, 28, and 56 days and age-matched controls. The protein expression of sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA) and its ryanodine receptor (RyR) were measured. The uptake of 45Ca2+ by SERCA, release by RyR, and extrusion by Na+/Ca2+ exchange (NCX) were determined. It was found that Ca2+ homeostasis and Ca2+ responses to {beta}-adrenoceptor stimulation reached a new equilibrium after 4 wk of CH. Ca2+ content in the sarcoplasmic reticulum (SR) was reduced, but cytosolic Ca2+ remained unchanged after CH. Expression of SERCA and its Ca2+ uptake, Ca2+ release via RyR, and NCX activity were suppressed by CH. The results indicate impaired Ca2+ handling, which may be responsible for the attenuated Ca2+ responses to {beta}-adrenoceptor stimulation in CH.

intracellular calcium ion concentration; calcium-adenosinetriphosphatase; ryanodine receptor; sodium/calcium exchange; sarcoplasmic reticulum; {beta}-adrenoceptor; chronic hypoxia


Address for reprint requests and other correspondence: T. M. Wong, Dept. of Physiology, Faculty of Medicine, Univ. of Hong Kong, 21 Sassoon Rd., Hong Kong, China (E-mail: wongtakm{at}hkucc.hku.hk).




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