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1 Pharmacology, Columbia University, New York, New York, United States
* To whom correspondence should be addressed. E-mail: pab4{at}columbia.edu.
While it is known that the incidence of atrial fibrillation increases with age, it is unknown whether there are changes in the intrinsic function of sodium currents in cells of the Aged atria. We studied right (RA) and left (LA) atrial cells from two groups of dogs, Adult and Aged( >8 yrs), to determine whether there is a change in the function of Na currents with Age. Whole cell voltage clamp techniques were used to compare the parameters of sodium currents in 2 cell groups. Immunocytochemical studies were completed for the sodium channel protein Nav1.5 to determine if there was structural remodeling of this protein with Age. In cells from Aged animals we found that Na+ currents(INa) are similar to those measured in Adult atria. However, Na+ current density of the Aged atria still differed depending on the atrial chamber with LA currents being larger than RA currents. Thus with Age the differences in INa density between atrial chambers remains. INa kinetic differences between Aged and Adult cells included a significant acceleration into the inactivated state and an enhancement of the rate of the use-dependent decrease in peak current in Aged RA cells. Finally there is no structural remodeling of the cardiac Na+ channel protein Nav1.5 in the Aged atrial cell. Thus with Age there is no change in sodium current density but there are subtle kinetic differences contributing to enhanced use dependence. There is no structural remodeling of the fast Na+ current protein with Age.
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