Aging-associated changes in whole cell K+ and L-type Ca2+ currents in rat ventricular myocytes
The effect of aging on cardiac membrane currents remains unclear. This study examined the inward rectifier K+ current ( I K1), the transient outward K+current ( I to), and the L-type Ca2+ channel current ( I Ca,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 I K1 with a greater slope conductance but displayed smaller steady-state I K1. Aged myocytes also had a greater I to with an increased rate of activation, but the I to inactivation kinetics, steady-state inactivation, and responsiveness to l-phenylephrine, an α1-adrenergic agonist, were unaltered. The magnitude of peak I Ca,L in aged myocytes was decreased and accompanied by a slower inactivation, but the I Ca,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 I toand I Ca,L but an increased I K1. These results demonstrate aging-associated changes in action potential, in morphology, and in I K1, I to, and I Ca,L of rat ventricular myocytes that possibly contribute to the decreased cardiac function of aged hearts.