Abstract

Transport of potassium by bullfrog choroid plexus was studied using tracers and ion-selective microelectrodes. 1) Tracers: We measured unidirectional uptakes of42K across each surface of the plexus, efflux of42K from loaded tissues, intracellular potassium pools, and [3H]-ouabain binding.42K uptake across the brush border membrane was composed of diffusional and saturable components. The saturable component exhibited kinetics of a two-site, model withKm's of 0.3mm and aVmax of 8 μmol cm−2 hr−1. Ouabain inhibited uptake across the brush border membrane with aKi of 1×10−7m. Ethacrynic acid, phloretin, amiloride, and low sodium concentrations inhibited uptake, whereas bicarbonate ions increased transport up to 100%. The rate of ouabain-sensitive uptake across the serosal surface was only 6% of that across the ventricular surface. The efflux of potassium across the brush border membrane could account for most of the efflux from the epithelium. Potassium was accumulated within the plexus to a concentration in excess of 100mm.42K in the extracellular compartments exchanged with 40–55% of the intracellular potassium. Ouabain bound to the brush border membrane with aKm of 8×10−7m, ak1 of 3.8×104 mol−1 min−1 and ak−1 of 3×10−2 min−1. Ouabain binding was blocked by cymarin and gitoxigin. 2) Electrodes: Under control conditions the intracellular electrical potential,Evc, was −45 mV and the apparent intracellular K+-concentration, Kc+, was 90mm. K+ ions appeared to be actively accumulated within the epithelium.Evc and Kc+ were followed under three experimental conditions: (i) treating the tissue with ouabain; (ii) varying the ventricular K+ concentration; and (iii) passing transmural currents. It is concluded that the permeability of the ventricular membrane to potassium (1–5 × 10−5 cm sec−1)_was much greater than the permeability of the serosal membrane and that the rate of K pumping into the epithelium was 0.35–0.55×10−9 mol cm−2 sec−1. 96% of the transmural current was paracellular, and the resistance of the serosal membrane was nine times greater than that of the ventricular membrane. Increasing Kc+ produced Nernstian changes inEvc andEKvc, but the cells only depolarized by 0.13 mV for each mV increase in the chemical potential of the ventricular solutions.

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