SUMMARY Erythrocyte sodium efflux as well as sodium, potassium, and water content were studied in 12 untreated men with uncomplicated essential hypertension and in 18 normotensive control subjects. In the patients with essential hypertension, the rate constant for total sodium efflux was significantly lower than in the nonnotensives (5.96-lfr* ± 0.45-10 • rain 1 TS 6.69*10 ' ± 0.49-lfr' mln ';/> < 0.005), which was due to a reduced ouabain-sensitire sodium efflux rate constant. Significant differences in total sodium efflux and ouabaln-sensitire sodium efflux, however, could not be demonstrated, since intracellular sodium concentrations, although insignificant, were higher in the patients with essential hypertension (6.11 ± 0.74 mmole/Hter vs 5.97 ± 0.66 mmole/llter. The rate constants for ouabain-lnsensltiTe sodium efflux, for ouabaln-lnsensitive furosemide-sensitire sodium efflux, and for passive (ouabain-insensitive furosemlde-insensitive) sodium efflux were similar in hypertensives and in normotenslves.The cause of the reduced rate constant for ouabaln-sensltive sodium efflux is not clear. However, as suggested for other types of altered erythrocyte transport mechanisms described recently, it might be determined genetically.
Red blood cell (RBC) phosphate release was linear for more than 1 h and dependent on the intracellular hydrolysis of organic phosphate esters. In uremics on chronic hemodialysis total phosphate release was significantly increased suggesting an elevated RBC energy metabolism. Ouabain-sensitive phosphate release, however, was decreased. For RBCs of controls and uremic subjects approximately 80% of inorganic phosphate liberated within the cell was recycled. Thus, RBC phosphate release represents 20% of intracellular phosphate ester metabolism. In uremia active electrolyte transport was diminished, suggesting an impaired Na-K-ATPase activity. It resulted in an increased RBC sodium and a decreased potassium concentration. The positive correlation between ouabain-sensitive rate constant for sodium efflux and ouabain-sensitive RBC phosphate release indicates that ouabain inhibition of phosphate elimination might be related to Na-K-ATPase. In RBCs of uremic subjects almost 4% of the increased energy metabolism was needed for active electrolyte transport mechanisms, in control RBCs 12% was required.
The effects of ouabain and furosemide on the unidirectional efflux of sodium and phosphate ions were studied in freshly drawn human red blood cells (RBCs). In the presence of physiologic concentrations of sodium and potassium the rate of sodium efflux was reduced by 74% due to ouabain sensitivity. Furosemide (1.0 mmol/l) reduced ouabain-insensitive sodium transport rate by a further 50%. Thus, 13% of total sodium efflux was inhibited by furosemide when ouabain was present. In the absence of ouabain, however, furosemide inhibited 31% of total sodium transport, indicating that it also affected ouabain-sensitive sodium efflux. Phosphate transfer of RBCs was almost 1.0 mmol/l RBCs per hour. Erythrocyte concentration of orthophosphate, however, was only 0.59 mmol/l RBCs. Organic phosphate esters must therefore have been cleaved to maintain constant phosphate elimination. The hydrolysis of adenosine triphosphate (ATP) by Na-K-ATPase might be involved because the phosphate transfer of almost 0.12 mmol/l RBCs per hour was ouabain sensitive. Furosemide reduced phosphate efflux by 50% due to reduction in passive permeability of the RBC membrane. Additional inhibition of any phosphate ester hydrolyzing enzymatic activity cannot, however, by excluded.
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