Key result
Cardiac-specific NCX knockout myocytes limit Ca2+ influx by reducing peak L-type Ca2+ current by 62% and abbreviating the action potential, while maintaining contractility.
Effect estimate: 62% reduction
In the absence of NCX, murine cardiomyocytes maintain contractility by reducing Ca2+ influx and increasing the gain of excitation-contraction coupling.
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NCX-independent Ca2+ handling may sustain contraction in mice; leaves open relevance to human heart failure.
Pott et al. (2005) studied Cardiac-specific Na+-Ca2+ exchanger (NCX) knockout. Cardiac-specific Na+-Ca2+ exchanger (NCX) knockout vs. Wild-type (WT) mice was evaluated on Peak L-type Ca2+ current (ICa) (62% reduction). Cardiac-specific NCX knockout myocytes limit Ca2+ influx by reducing peak L-type Ca2+ current by 62% and abbreviating the action potential, while maintaining contractility.
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