The relative decrease of the Na+-K+-ATPase α2-isoform during the transition from compensated to decompensated left ventricular hypertrophy may contribute to decompensation and arrhythmias.
α2-isoform reduction may promote decompensation; animal data leave open human relevance and therapeutic targeting.
Disturbance in ionic gradient across sarcolemma may lead to arrhythmias. Because Na + -K + -ATPase regulates intracellular Na + and K + concentrations, and therefore intracellular Ca 2+ concentration homeostasis, our aim was to determine whether changes in the Na + -K + -ATPase α-isoforms in guinea pigs during transition from compensated (CLVH) to decompensated left ventricular hypertrophy (DLVH) were concomitant with arrhythmias. After 12- and 20-mo aortic stenosis, CLVH and DLVH were characterized by increased mean arterial pressure (30% and 52.7%, respectively). DLVH differed from CLVH by significantly increased end-diastolic pressure (34%), decreased sarco(endo)plasmic reticulum Ca 2+ -ATPase (−75%), and increased Na + /Ca 2+ exchanger (25%) mRNA levels and by the occurrence of ventricular arrhythmias. The α-isoform (mRNA and protein levels) was significantly lower in DLVH (2.2 ± 0.2- and 1.4 ± 0.15-fold, respectively, vs. control) than in CLVH (3.5 ± 0.4- and 2.2 ± 0.13-fold, respectively) and was present in sarcolemma and T tubules. Changes in the levels of α 1 - and α 3 -isoform in CLVH and DLVH appear physiologically irrelevant. We suggest that the increased level of α 2 -isoform in CLVH may participate in compensation, whereas its relative decrease in DLVH may enhance decompensation and arrhythmias.
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Trouvé et al. (2000) studied this question.
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