The study provides a theoretical explanation for the propranolol-induced potassium leak in red cells, suggesting it occurs via free diffusion driven by a diffusion potential, which may relate to its antiarrhythmic effects.
Answers are grounded in this paper and cite their sources.
No immediate clinical implications for propranolol; leaves open whether diffusion potentials mediate its antiarrhythmic effects in vivo.
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.
No takes yet. Share an insight, caveat, or question.
Glynn et al. (1972) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: