How extracellular potassium affects intracellular sodium pool in human erythrocytes.

In order to evaluate the regulation of intracellular sodium and potassium balance, we investigated the Na+/K(+)-ATPase independent 22Na+ uptake and concentrations of Na+ in erythrocytes from eleven normal subjects. The experiments were performed with the purified erythrocyte suspensions in different assay buffers containing (i) 5 mEq/L KCl and varying amounts of NaCl (5 to 100 mEq/L); and (ii) a range of KCl (5 to 100 mEq/L) and a constant amount of NaCl (5 mEq/L). These erythrocyte suspensions were incubated at 37 degrees C for 30 minutes to assess ouabain insensitive 22Na+ uptake. Erythrocytes (2.0 x 10(9)/mL) showed an uptake of 2.03 to 0.88%, and 2.00 to 1.15% of the total 22Na+ present in the media under these experimental conditions, respectively. The 22Na+ uptake by erythrocytes was decreased by a gradual increase of either NaCl or KCl in the assay buffers. Erythrocytes in the experimental condition (i) showed an increase in intracellular sodium [Na+]i from 8.29 to 10.06 mEq/L. However in the condition (ii), KCl up to 20 mEq/L extracellularly caused a limited inhibition of [Na+]i accumulation (8.29 to 8.23 mEq/L), however, when KCl was raised extracellularly greater than 20 mEq/L it enhanced [Na+]i slowly (8.23 to 9.19 mEq/L). When NaCl 20, 50 and 100 mEq/L were replaced by an equivalent amount of KCl in the assay buffers, this extracellular K+ prevented 7, 6 and 10% [Na+]i accumulation, respectively. We also found that bicarbonate induced ouabain resistance 22Na+ influx was both inhibited and stimulated depending upon the amount of KCl in the assay media.(ABSTRACT TRUNCATED AT 250 WORDS)