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Sodium current function in adult and aged canine atrial cells

Department of Pharmacology, Center for Molecular Therapeutics, Columbia University, New York, New York

Submitted 17 January 2006 ; accepted in final form 17 March 2006

The incidence of atrial fibrillation increases with age, but it is unknown whether there are changes in the intrinsic function of Na⁺ currents in cells of the aged atria. Thus, we studied right (RA) and left (LA) atrial cells from two groups of dogs, adult and aged (>8 yr), to determine the change in Na⁺ currents with age. In this study all dogs were in normal sinus rhythm. Whole cell voltage clamp techniques were used to compare the Na⁺ currents in the two cell groups. Immunocytochemical studies were completed for the Na⁺ channel protein Na_v1.5 to determine whether there was structural remodeling of this protein with age. In cells from aged animals, we found that Na⁺ currents are similar to those we measured in adult atria. However, Na⁺ current (I_Na) density of the aged atria differed depending on the atrial chamber with LA cell currents being larger than RA cell currents. Thus with age, the difference in I_Na density between atrial chambers remains. I_Na kinetic differences between aged and adult cells included a significant acceleration into the inactivated state and an enhanced use-dependent decrease in peak current in aged RA cells. Finally, there is no structural remodeling of the cardiac Na⁺ channel protein Na_v1.5 in the aged atrial cell. In conclusion, with age there is no change in I_Na density, but there are subtle kinetic differences contributing to slight enhancement of use dependence. There is no structural remodeling of the fast Na⁺ current protein with age.

ion channels; remodeling; arrhythmias; atrial fibrillation; age

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