Key result
Selective inhibition of the alpha2-isoform of the Na+/K+-ATPase with 0.3 microM ouabain induced a 40% increase in contractility in field-stimulated rat cardiomyocytes without increasing global [Na+]i.
Why the study?
Does selective inhibition of the Na+/K+-ATPase alpha2-isoform increase contractility in isolated rat cardiomyocytes?
Population
Isolated cardiomyocytes from Wistar rats
Comparison
Selective inhibition of the Na+/K+-ATPase… vs Control and detubulated cardiomyocytes
Design
Preclinical
Authors
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Selective alpha2-Na/K-ATPase inhibition boosts rat cardiomyocyte contractility without Na+i rise; leaves open human translation and therapeutic potential.
Does selective inhibition of the Na+/K+-ATPase alpha2-isoform increase contractility in isolated rat cardiomyocytes?
The alpha2-isoform of the Na+/K+-ATPase is functionally coupled to the Na+/Ca2+-exchanger and regulates calcium handling and contractility without changing global intracellular sodium concentration.
Swift et al. (2007) studied this question. Ouabain (selective inhibition of alpha2-isoform) vs. Control (uninhibited/detubulated cardiomyocytes) was evaluated on NKA pump current (I(pump)) and contractility. Selective inhibition of the alpha2-isoform of the Na+/K+-ATPase with 0.3 microM ouabain induced a 40% increase in contractility in field-stimulated rat cardiomyocytes without increasing global [Na+]i.
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