American Journal of Physiology-Cell Physiology · 2003 · 38 citations · 37 references
Life SciencesCardiologyPhysiologyCalcium HomeostasisCellular BiochemistryElectrophysiologyCalcium MetabolismCardiac Ion ChannelsCardiac PhysiologyCellular Responses To HypoxiaHypoxia PhysiologyIntracellular Calcium SignalingCalcium Handling In CardiomyocytesCardiac Calcium HandlingElectrical StimulationHypoxiaIntracellular Calcium HomeostasisRyanodine Receptor RegulationRyanodine ReceptorsSarcoplasmic Reticulum Calcium Atpases
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.
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Theory of excitation-contraction coupling in cardiac muscle
Michael D. Stern · Biophysical Journal · 1992 · 655 citations
Hui He, Frank J. Giordano, Randa Hilal-Dandan et al. · Journal of Clinical Investigation · 1997 · 325 citations · Full text