Effect of extracellular potassium on the loss of potassium from human red blood cells treated with propranolol

The Ca++-dependent propranolol-induced increase of K+ permeability of human red blood cells, well documented in previous studies, was found to depend on extracellular K+. This was shown by studying the passive transport of 86Rb and the loss of bulk cellular K+ in both K+-free and K+-containing media. The maximal effect of propranolol was achieved with 5–10 mM K+ in incubation media. The external K+ could be substituted with TI+, but not with Na+. When added after propranolol, extracellular K+ failed to initiate the effect of propranolol on membrane permeability. The cell/medium distribution of permeant 204TI showed that the propranolol-induced increase of K+ permeability did not result in considerable hyperpolarization of the red blood cell membrane. The data obtained seem to be more consistent with a counter-transport model for explaining the propranolol effect than with a mechanism based on free diffusion of K+ through the membrane.