Does sodium intake modify red cell Na+ transporters in normal and hypertensive subjects?

Abnormalities in sodium transport in red blood cells (RBC) have been reported in hypertensive subjects. Uncertain from previous studies is whether the level of sodium intake per se might influence the level of these transporters. This study was designed to answer that question by evaluating the level of activity of three RBC sodium transporters in fourteen normotensive and twenty-six hypertensive subjects studied twice--once while in balance on a 10 mEq and once while in balance on a 200 mEq sodium intake. There was no significant difference in the maximal velocity (Vmax) of the sodium pump or the cell sodium and potassium content in normotensive or hypertensive subjects, nor did sodium intake influence these factors. Li-Na countertransport activity was significantly (P less than .01) higher in the hypertensive than in the normotensive subjects. However, sodium intake did not influence the Vmax of this transporter in either group. In contrast, sodium efflux through the Na-K-Cl cotransporter was significantly influenced (P less than .03) by the level of sodium intake, but only in the hypertensive subjects. On the high sodium intake, both the Km and the Vmax were significantly elevated (P less than .03) compared to their levels on the low sodium diet. Additionally, only on the high salt diet did hypertensives have significantly higher levels of activity than normotensives (P less than .03). Thus, Na-K-Cl cotransport activity is influenced by the level of sodium intake, suggesting that caution needs to be exercised in interpreting the level of activity of this transporter unless the level of sodium intake is fixed and known.