Influence of race, sex, and blood pressure on erythrocyte sodium transport in humans

Abstract

Sodium transport of erythrocytes from normotensive and essential hypertensive subjects was evaluated by determining ouabain-sensitive and ouabain-insensitive sodium efflux rates, Na+-Li+ countertransport rates, Li+-K+ cotransport rate constants (lithium replacing sodium), intracellular sodium concentrations, and the number of Na+, K+-adenosine triphosphatase (ATPase) sites per erythrocyte. Subjects included men and women, blacks and whites. Hypertensive subjects had significantly higher sodium transport than did normotensive subjects for ouabain-sensitive sodium efflux (p < 0.025) and Na+-Li+ countertransport (p < 0.001). Sexual differences were noted for ouabain-sensitive (p < 0.001) and ouabain-insensitive (p < 0.001) sodium efflux, for intracellular sodium concentration (p < 0.025), and for the Li+-K+ cotransport rate constant (p < 0.005), all with higher values for men than for women. Racial differences were noted for ouabain-insensitive sodium efflux (p < 0.005), Na+-Li+ countertransport (p < 0.001), and the Li+-K+ cotransport rate constant (p < 0.001); values were higher in whites than blacks for all three measurements. The number of [3H]ouabain binding sites was lower for blacks (p < 0.001) and the intracellular sodium concentration was higher for blacks (p < 0.001). Among all subjects, significant (p < 0.001) correlations were found between intracellular sodium concentration and the number of Na+, K+-ATPase sites per erythrocyte (r = -0.78) and between the ouabain-sensitive sodium efflux per site and intracellular sodium concentration (r = 0.85, p < 0.001). The values for sodium efflux, intracellular sodium, and the number of adenosine triphosphatase sites per red blood cell were used to calculate a second-order rate constant that was significantly (p = 0.011) higher among hypertensive than among normotensive subjects. The results indicate that significant differences in sodium handling are present in erythrocytes of hypertensive subjects and suggest that further elucidation of these abnormalities may provide insights into the pathogenesis of essential hypertension.