title: Characterization of a sodium pump-induced hyperpolarization in isolated human atrium.
abstract: Specimens of right atrial appendage from 106 patients were incubated in cold Tyrode solution, and transmembrane resting potentials (Em) were recorded during rewarming at selected temperatures. Rewarming caused a transient hyperpolarization to develop. The hyperpolarization had a temperature threshold between 17 and 22 degrees C and was inhibited by acetylstrophanthidin. Acetylcholine (ACh) induced a depolarization during early rewarming in 7, 10, 20, and 40 mM K+, indicating that Em hyperpolarized to a potential negative to the equilibrium potential for K+. ACh had no effect after some decline of Em, and hyperpolarization was induced by ACh when Em had reached steady state. The relationship between [K+] in the bulk phase of the superfusate [( K]b) and the "reversal potentials" for the ACh effect was log linear and had a slope of 61.7 mV per tenfold change in [K]b. The relationship between [K]b and hyperpolarization was studied in the presence of 0.5 mM Ba2+. The apparent [K]b resulting in half-maximal pump-induced hyperpolarization was 1.3 mM. The data indicate that human atrium can pump Na+ electrogenically and that the characteristics of the Na+ pump-induced hyperpolarization resemble those described for cardiac tissue from several other mammalian species.
mesh_terms: D000368:Aged; D001464:Barium / Q000494:pharmacology; D004594:Electrophysiology; D006325:Heart Atria; D006706:Homeostasis; D006358:Hot Temperature; D006801:Humans; D007473:Ion Channels / Q000502:physiology*; D008564:Membrane Potentials; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D009994:Osmolar Concentration; D011188:Potassium / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism*; D013327:Strophanthidin / Q000031:analogs & derivatives / Q000494:pharmacology; D013696:Temperature
chemical_list: D007473:Ion Channels; D001464:Barium; D013327:Strophanthidin; D012964:Sodium; C004681:acetylstrophanthidin; D011188:Potassium