Aging-associated changes in whole cell K+ and L-type Ca2+ currents in rat ventricular myocytes

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Abstract
The effect of aging on cardiac membrane currents remains unclear. This study examined the inward rectifier K+ current (IK1), the transient outward K+current (Ito), and the L-type Ca2+ channel current (ICa,L) in ventricular myocytes isolated from young adult (6 mo) and aged (>27 mo) Fischer 344 rats using whole cell patch-clamp techniques. Along with an increase in the cell size and membrane capacitance, aged myocytes had the same magnitude of peak IK1 with a greater slope conductance but displayed smaller steady-stateIK1. Aged myocytes also had a greaterIto with an increased rate of activation, but theIto inactivation kinetics, steady-state inactivation, and responsiveness to l-phenylephrine, an α1-adrenergic agonist, were unaltered. The magnitude of peak ICa,L in aged myocytes was decreased and accompanied by a slower inactivation, but theICa,L steady-state inactivation was unaltered. Action potential duration in aged myocytes was prolonged only at 90% of full repolarization (APD90) when compared with the action potential duration of young adult myocytes. Aged myocytes from Long-Evans rats showed similar changes in Itoand ICa,L but an increasedIK1. These results demonstrate aging-associated changes in action potential, in morphology, and inIK1, Ito, andICa,L of rat ventricular myocytes that possibly contribute to the decreased cardiac function of aged hearts.

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