To investigate the role of the electrogenic Na-K
+ pump in the resting membrane of "diseased" or "depolarized" human atrial muscles, intracellular K
++ activity (a
iK+) and resting membrane potential (
Vm) were simultaneously measured using double-barreled K
++-selective microelectrodes. Under perfusion with normal Tyrode's solution (37°C) containing 5.4mM [K
+]
0,
Vmaveraged -43.9±1.4mV, and a
iK+ was 99.7±1.3mM (mean±S.E.,
n=33). The a
iK+ was comparable to that of atrial muscles obtained from other intact mammalian species. In 5.4mM [K
+]o, dihydro-ouabain (DHO) at concentrations of 10
-6 and 10
-5M significantly decreased a
iK+ and depolarized Vm. Similar decreases in a
iK+ were observed when [K
+]o was decreased from 5.4 to 0.5mM or when the temperature of the perfusing solution was decreased from 37 to 22°C. Upon returning [K
+]o from 0.5 to 5.4mM at 37°C, a
iK+ increased,
Vmhyperpolarized markedly for about 3min, and this was followed by less marked levels of hyperpolarization in the steady state. The high [K
+]o-induced increases in a
iK+ were inhibited in the presence of DHO, and at low temperature (22°C). Isoproterenol (10
-7M) increased a
iK+ and hyperpolarized Vm. Acetylcholine (10
-5M) hyperpolarized
Vmwith no change in a
iK+. The rate of reduction of Na+-efflux during application of DHO (10
-5M) was calculated based on the change in a
iK+ and surface-to-volume ratio of the cell measured electronmicroscopically in the same tissue, and estimated to be 2.6 to 3.8pmol/(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 a
iK+ within a physiological range.
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