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Abstract

In the presence of 8 mm external Ca⁺⁺, the K⁺ permeability of human red cell ghosts increases provided K⁺ is also present in the medium. This increase does not represent K⁺/K⁺ exchange but a stimulation of net K⁺ efflux. The stimulation is halfmaximal at 0.7±0.15 mm (n=5). At concentrations above 4.0 mm, external K⁺ inhibits net K⁺ efflux. Similar stimulatory and inhibitory effects of external K⁺ were also observed in intact cells after exposure to Pb⁺⁺ or to Ca⁺⁺ in the presence of fluoride, iodoacetate plus adenosine, or propranolol, suggesting that a common K⁺-activated K⁺-specific transfer system may be involved under all of these various circumstances. Internal K⁺ also stimulates net K⁺ efflux from ghosts, but it is uncertain whether internal K⁺ is an absolute requirement for the K⁺ permeability increase. In contrast to external Na⁺ which slightly stimulates K⁺ efflux, internal Na⁺ inhibits. The inhibition by internal Na⁺ is abolished by sufficiently high concentrations of external K⁺, showing that K⁺ binding to the outer membrane surface and Na⁺ binding to the internal surface are mutually interdependent. In red cell ghosts the Ca⁺⁺-K⁺-stimulated net K⁺ efflux increases with increasing pH until a plateau is reached between pH 7.2 and 8.0. In fluoride-poisoned intact cells, the Ca⁺⁺-K⁺ stimulated flux passes through a maximum around pH 6.8. Neither internal nor external Mg⁺⁺ interferes with the combined effects of Ca⁺⁺ and K⁺. Similarly, external EDTA has no influence at concentrations which are far lower than the Ca⁺⁺ concentration required to produce a maximal response. In contrast, low concentrations of internal EDTA prevent the permeability change