Erythrocyte Na Flux in a Patient with Bartter's Syndrome

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Abstract
Erythrocyte ghost Na flux, Na + K dependent ATPase, and intracellular electrolytes have been measured in a patient with Bartter's syndrome, JM, and contrasted with similar measurements in patients with primary and secondary hyperaldosteronism. JM was found to have increased active Na transport, increased passive outward leak of Na, elevated Na + K dependent ATPase, and increased erythrocyte intracellular Na concentrations. Mean normal rate constant for Na active transport was 0.365 ± 0.002/hr (sem), with a passive leak rate constant/hr of 0.221±0.008. Na + K dependent ATPase activity was 0.053 ± 0.003 pinole P/mg protein/10 min and intracellular erythrocyte Na concentration was 8.7 ± 0.238 mEq/kg RBC. The corresponding values in JM were 0.92 ± 0.086, 0.54 ± 0.017, 0.098 ± 0.010 and 12.4 ± 0.84. The differences from control values were all significant at the 99% level of confidence. The efflux studies in erythrocyte ghosts were corroborated by Na efflux and influx studies in intact red blood cells. In contrast, patients with primary or secondary hyperaldosteronism demonstrated increased erythrocyte outward active transport of Na but no change in the passive Na efflux. Their erythrocyte Na concentrations were normal or low; Na + K dependent ATPase activities were high. These findings suggest a primary increase in membrane permeability to Na in JM, with a compensatory increase in active outward Na transport. Such an increase in membrane permeability to Na in renal cells, erythrocytes and other cells would explain the secondary increase in aldosterone secretion and other alterations in physiologic mechanisms in Bartter's syndrome.

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