title: Unaffected electrogenic Na-K pump activity in "diseased" human atrial fibers, as assessed by intracellular K+ activity.
abstract: 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 [K]o, 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 [K]o, 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 [K]o 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 [K]o 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 [K]o-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.
authors.affiliation: Department of Physiology, Faculty of Medicine, Medical College of Oita, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Sako
authors.forename: S
authors.initials: S
authors.lastname: Imanishi
authors.forename: M
authors.initials: M
authors.lastname: Arita
authors.forename: T
authors.initials: T
authors.lastname: Shimada
authors.forename: T
authors.initials: T
authors.lastname: Hadama
authors.forename: Y
authors.initials: Y
authors.lastname: Uchida
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D016275:Atrial Function; D001693:Biological Transport, Active; D002648:Child; D002675:Child, Preschool; D004553:Electric Conductivity; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology; D008564:Membrane Potentials / Q000502:physiology; D008854:Microscopy, Electron; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D010042:Ouabain / Q000031:analogs & derivatives / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000502:physiology*; D015398:Signal Transduction; D015222:Sodium Channels / Q000187:drug effects / Q000502:physiology*; D013696:Temperature
chemical_list: D015221:Potassium Channels; D015222:Sodium Channels; C000977:dihydroouabain; D010042:Ouabain; D007545:Isoproterenol