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Prolonged action potential duration (APD) and decreased transient outward K+ current (I to ) as a result of decreased expression of Kv4.2 and Kv4.3 genes are commonly observed in heart disease. We found that treatment of cultured neonatal rat ventricular myocytes with Heteropoda Toxin3 , a blocker of cardiacI to , induced hypertrophy as measured using cell membrane capacitance and3 H-leucine uptake. To dissect the role of specificI to -encoding genes in hypertrophy,I to was selectively reduced by overexpressing mutant dominant-negative (DN) transgenes.I to amplitude was reduced equally (by about 50%) by overexpression of DN Kv1.4 (Kv1.4 N) or DN Kv4.2 (either Kv4.2 N or Kv4.2 W362F), but only DN Kv4.2 prolonged APD duration (at 1 Hz) and induced myocyte hypertrophy. This hypertrophy was prevented by coexpressing wild-type Kv4.2 channels (Kv4.2 F) with the DN Kv4.2 genes, suggesting the hypertrophy is due toI to reduction and not nonspecific effects of transgene overexpression. The hypertrophy caused by reductions of Kv4.x -basedI to was associated with increased activity of the calcium-dependent phosphatase, calcineurin, and could be prevented by coinfection with Ad-CAIN, a specific calcineurin inhibitor. The hypertrophy and calcineurin activation induced by Kv4.2 N infection were prevented by blocking Ca2+ entry and excitability with verapamil or high [K+ ]o . Our studies suggest that reductions of Kv4.2/3 -basedI to play a role in hypertrophy signaling by activation of calcineurin.

Reduction of I to Causes Hypertrophy in Neonatal Rat Ventricular Myocytes

Reduction of I _to Causes Hypertrophy in Neonatal Rat Ventricular Myocytes