Characterization of a sodium pump-induced hyperpolarization in isolated human atrium.
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.
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
D007473:Ion Channels; D001464:Barium; D013327:Strophanthidin; D012964:Sodium; C004681:acetylstrophanthidin; D011188:Potassium