Red cell lithium-sodium countertransport and sodium-potassium cotransport in patients with essential hypertension.

Abstract

Alterations in sodium countertransport and cotransport have been reported in red cells of patients with essential hypertension. We have investigated the relationship between these two systems by performing simultaneous measurements of the maximal rates of lithium-sodium (Li1-Na0) countertransport and outward sodium-potassium (Na-K) cotransport in red cells from normotensive and hypertensive subjects. Li1-Na0 countertransport was assayed by measuring the Na0-stimulated Li efflux from cells loaded to contain 10 mmoles Li per liter of cells by incubation in isotonic LiCl. Na-K cotransport was assayed by measuring the furosemide-sensitive component of Na and K efflux into magnesium-sucrose medium from cells loaded by the p-chloromercuribenzene sulfonic acid (PCMBS) procedure to obtain 50 mmoles of both ions per liter of cells. The mean values (+/- SE) for 16 normotensives and 22 hypertensives were (mmole/liter cells x hour): Na countertransport = 0.29 +/- 0.02 vs 0.51 +/- 0.03 (p less than 0.001); Na cotransport = 0.30 +/- 0.03 vs 0.51 +/- 0.05 (p less than 0.005); and K cotransport = 0.34 +/- 0.03 vs 0.60 +/- 0.04 (p less than 0.005). Li1-Na0 countertransport correlated significantly with Na cotransport (r = 0.50, n = 38, p less than 0.005) and K cotransport (r = 0.57, p less than 0.005). This observation suggests that both transport systems are somehow regulated to be more active in this group of hypertensive patients. The increased cotransport in hypertensive patients is also apparent from two other measurements of Na and K fluxes in red cells suspended in Na medium. First, the furosemide-sensitive net Na efflux into Na medium was (mean +/- SE) 0.25 +/- 0.05 in 10 normotensive subjects and 0.50 +/- 0.09 in 12 hypertensive patients. Second, the furosemide-sensitive net K efflux into Na medium was (mean +/- SE) 0.25 +/- 0.04 in 13 normotensive subjects and 0.43 +/- 0.04 in 16 hypertensive patients (p less than 0.005). We conclude that mean values for both Na countertransport and Na-K cotransport are significantly higher in the group of hypertensives than in the group of normal control subjects.