Na+/K+-ATPase 2-isoform preferentially modulates Ca2+ transients and sarcoplasmic reticulum Ca2+ release in cardiac myocytes
Key result
Ouabain-induced NKA-α2 inhibition in wild-type mice significantly increased Ca2+ transients and fractional SR Ca2+ release, an effect not seen with NKA-α1 block in SWAP mice.
Population
Cardiac myocytes from wild-type mice, SWAP mice, and transgenic mice
Comparison
Ouabain at low concentration vs Baseline and comparison between WT and SWAP mice
Design
Preclinical
Authors
Discussion
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Member takes
Implication
Mouse data suggest NKA-α2 predominance in Ca2+ release; leaves open clinical relevance in human heart failure.
Structured PICO
P
Population
Cardiac myocytes from wild-type (WT) mice, SWAP mice (NKA-α1 ouabain sensitive, NKA-α2 ouabain resistant), and transgenic mice (both NKA-α1 and NKA-α2 ouabain resistant)
I
Intervention
Ouabain at low concentration
C
Comparator
Baseline and comparison between WT and SWAP mice
O
Outcome
Ca2+ transients and fractional sarcoplasmic reticulum (SR) Ca2+ releasesurrogate
The NKA-α2 isoform plays a more prominent role than NKA-α1 in modulating cardiac myocyte sarcoplasmic reticulum Ca2+ release.
Cite This Study
Despa et al. (2012) studied this question. Ouabain vs. SWAP mice (selective NKA-α1 block) was evaluated on Ca2+ transients and fractional sarcoplasmic reticulum (SR) Ca2+ release. Ouabain-induced NKA-α2 inhibition in wild-type mice significantly increased Ca2+ transients and fractional SR Ca2+ release, an effect not seen with NKA-α1 block in SWAP mice.