Red cell sodium metabolism in human hypertension - abstract

ABSTRACT

A derangement in cell sodium homeostasis has been reputed to be the cause of primary hypertension in man. This hypothesis is supported by findings of raised intracellular sodium and suppressed sodium pump activity. These findings, however, are not universal. These experiments were designed to measure red cell sodium and potassium content and sodium transport activity as well as to define the role of plasma in these transport activities. Twelve hypertensives and 27 normotensive controls were subjected to venipuncture. Red cells were separated from plasma and the cellular content of sodium and potassium was measured. Na efflux from loaded cells was used to measure sodium pump activity and contransport. Red cell sodium content was slightly higher in hypertensive patients (10.4ñ2.8 vs 8.7ñ2.1 mMOl/l RBC, p<.05). Red cell potassium was the same in both groups (110ñ7 vs 113ñ8 mMOl/l RBC). Ouabain-sensitive sodium efflux, a measure of sodium pump activity, was the same in hypertensives and normotensives (6.69ñ2.57 vs 6.57ñ2.34 mMol/l /RBC/h). Plasma incubation produced an across-the-board reduction in sodium transport activities. Ouabain-sensitive efflux was 5.79ñ3.05 vs 4.23ñ2.66, and contransport, 0.57ñ0.28 vs 0.63ñ0.27 mMol/l RBC/h in hypertensives and normotensives respectively. We conclude that red cell sodium homeostasis is virtually identical in hypertensives and normotensives and that a circulating inhibitor is present to the same degree in both their plasmas. These data do not support the hypothesis that essential hypertension is causally associated with derangements of cell sodium metabolism (AU)