Regulation of Ca2Â + signaling by acute hypoxia and acidosis in rat neonatal cardiomyocytes

Our studies suggest that acute hypoxia suppresses ICa in rapidly inactivating cell population by a mechanism involving Ca2 +-dependent inactivation, while compromised mitochondrial Ca2 + uptake seems also to contribute to ICa suppression in slowly inactivating cell population. Proximity of cellular Ca2 + pools to sarcolemmal Ca2 + channels may contribute to the variability of inactivation kinetics of ICa in the two cell populations, while acidosis suppression of ICa appears mediated by proton-induced block of the calcium channel.