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Postnatal development has a marked effect on ventricular repolarization in mice

Research Center, Montreal Heart Institute, and Faculty of Pharmacy, University of Montreal, Montreal, Quebec, Canada

Submitted 1 May 2007 ; accepted in final form 2 August 2007

To better understand the mechanisms that underlie cardiac repolarization abnormalities in the immature heart, this study characterized and compared K⁺ currents in mouse ventricular myocytes from day 1, day 7, day 20, and adult CD1 mice to determine the effects of postnatal development on ventricular repolarization. Current- and patch-clamp techniques were used to examine action potentials and the K⁺ currents underlying repolarization in isolated myocytes. RT-PCR was used to quantify mRNA expression for the K⁺ channels of interest. This study found that action potential duration (APD) decreased as age increased, with the shortest APDs observed in adult myocytes. This study also showed that K⁺ currents and the mRNA relative abundance for the various K⁺ channels were significantly greater in adult myocytes compared with day 1 myocytes. Examination of the individual components of total K⁺ current revealed that the inward rectifier K⁺ current (I_K1) developed by day 7, both the Ca²⁺-independent transient outward current (I_to) and the steady-state outward K⁺ current (I_ss) developed by day 20, and the ultrarapid delayed rectifier K⁺ current (I_Kur) did not fully develop until the mouse reached maturity. Interestingly, the increase in I_Kur was not associated with a decrease in APD. Comparison of atrial and ventricular K⁺ currents showed that I_to and I_Kur density were significantly greater in day 7, day 20, and adult myocytes compared with age-matched atrial cells. Overall, it appears that, in mouse ventricle, developmental changes in APD are likely attributable to increases in I_to, I_ss, and I_K1, whereas the role of I_Kur during postnatal development appears to be less critical to APD.

mouse; ventricle; K⁺ currents; K⁺ channels; action potential

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