Article ID Journal Published Year Pages File Type
8473575 Journal of Molecular and Cellular Cardiology 2018 43 Pages PDF
Abstract
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.
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