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1 Institute of Health Sciences, Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS) & Shanghai Jiao Tong University School of Medicine (SJTUSM), Shanghai, China
2 Institute of Health Sciences, SJTUSM & SIBS, CAS, Shanghai, China
3 Physiological Laboratory of Hypoxia, SIBS, CAS, Shanghai, China
4 Institute of Health Sciences, Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS) & Shanghai Jiao Tong University School of Medicine (SJTUSM), Shanghai, China; Institute of Health Sciences, SJTUSM & SIBS, CAS, Shanghai, China
* To whom correspondence should be addressed. E-mail: htyang{at}sibs.ac.cn.
We have previously demonstrated that intermittent high altitude (IHA) hypoxia significantly attenuates ischemia-reperfusion (I/R)-induced excessive increase in the resting [Ca2+]i. Since the sarcoplasmic reticulum (SR) and Na+/Ca2+ exchange (NCX) play crucial roles in regulating [Ca2+]i and both are in dysfunction during I/R, we tested the hypothesis in the present study that IHA hypoxia may prevent I/R-induced Ca2+ overload by maintainting Ca2+ homeostasis via SR and NCX mechanisms. We thus determined the dynamics of Ca2+ transients and cell shortening during preischemia and I/R in ventricular cardiomyocytes from normoxic and IHA hypoxic rats. IHA hypoxia did not affect the preischemic dynamics of Ca2+ transients and cell shortening, but it significantly suppressed the I/R-induced increase in the resting [Ca2+]i and attenuated the depression of the Ca2+ transients and cell shortening during reperfusion. Moreover, IHA hypoxia significantly attenuated I/R-induced depression of the protein contents of SR Ca2+ release channels/ryanodine receptors (RyRs) and Ca2+-pump ATPase (SERCA2) and SR Ca2+ release and uptake. In addition, a delayed decay of Ca2+ transients seen at ischemia was accompanied with markedly inhibited NCX currents, which were prevented by IHA hypoxia. These findings indicate that IHA hypoxia may preserve Ca2+ homeostasis and contraction by preserving RyRs and SERCA2 proteins and NCX activity during I/R.
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