Nature of the calcium dependent potassium leak induced by (+)-propranolol, and its possible relevance to the drug's antiarrhythmic effect.
1. Manninen (1970) recently reported that in the presence of calcium ions, (+)-propranolol causes a massive loss of potassium ions from human red cells, together with a marked inward ;counter-transport' of potassium ions from the medium.2. This paper shows, theoretically, that counter-transport of the kind he observed may be accounted for by the setting up of a diffusion potential across the cell membrane and does not imply that, under the influence of propranolol, potassium ions cross the membrane by some process other than free diffusion.3. The physiological and pharmacological significance of this interpretation of Manninen's findings is briefly discussed.
D000889:Anti-Arrhythmia Agents / Q000494:pharmacology*; D001692:Biological Transport / Q000187:drug effects; D002118:Calcium / Q000494:pharmacology*; D002463:Cell Membrane Permeability; D002712:Chlorides / Q000097:blood; D004058:Diffusion; D004912:Erythrocytes / Q000378:metabolism; D006801:Humans; D008433:Mathematics; D008564:Membrane Potentials; D011188:Potassium / Q000097:blood*; D011194:Potassium Isotopes; D011433:Propranolol / Q000494:pharmacology*
D000889:Anti-Arrhythmia Agents; D002712:Chlorides; D011194:Potassium Isotopes; D011433:Propranolol; D011188:Potassium; D002118:Calcium