Unaffected electrogenic Na-K pump activity in "diseased" human atrial fibers, as assessed by intracellular K+ activity.

To investigate the role of the electrogenic Na-K pump in the resting membrane of "diseased" or "depolarized" human atrial muscles, intracellular K+ activity (aiK) and resting membrane potential (Vm) were simultaneously measured using double-barreled K(+)-selective microelectrodes. Under perfusion with normal Tyrode's solution (37 degrees C) containing 5.4 mM Ko, Vm averaged -43.9 +/- 1.4 mV, and aiK was 99.7 +/- 1.3 mM (mean +/- S.E., n = 33). The aiK was comparable to that of atrial muscles obtained from other intact mammalian species. In 5.4 mM Ko, dihydro-ouabain (DHO) at concentrations of 10(-6) and 10(-5) M significantly decreased aiK and depolarized Vm. Similar decreases in aiK were observed when Ko was decreased from 5.4 to 0.5 mM or when the temperature of the perfusing solution was decreased from 37 to 22 degrees C. Upon returning Ko from 0.5 to 5.4 mM at 37 degrees C, aiK increased, Vm hyperpolarized markedly for about 3 min, and this was followed by less marked levels of hyperpolarization in the steady state. The high Ko-induced increases in aiK were inhibited in the presence of DHO, and at low temperature (22 degrees C). Isoproterenol (10(-7) M) increased aiK and hyperpolarized Vm. Acetylcholine (10(-5) M) hyperpolarized Vm with no change in aiK. The rate of reduction of Na(+)-efflux during application of DHO (10(-5) M) was calculated based on the change in aiK and surface-to-volume ratio of the cell measured electronmicroscopically in the same tissue, and estimated to be 2.6 to 3.8 pmol/(cm2.s), close to the value reported for Purkinje fibers excised from intact animals. We conclude that the Na-K pump functions normally even in "diseased" human atrial muscles, thereby keeping aiK within a physiological range.