Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8473575 | Journal of Molecular and Cellular Cardiology | 2018 | 43 Pages |
Abstract
Our studies suggest that acute hypoxia suppresses ICa in rapidly inactivating cell population by a mechanism involving Ca2Â +-dependent inactivation, while compromised mitochondrial Ca2Â + uptake seems also to contribute to ICa suppression in slowly inactivating cell population. Proximity of cellular Ca2Â + pools to sarcolemmal Ca2Â + 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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Authors
José-Carlos Fernández-Morales, Martin Morad,