Abstract

To test whether leucocyte sodium pumps function abnormally in patients with essential hypertension specific tritium-ouabain binding (number of pumps) and ouabain sensitive uptake of rubidium-86 (86Rb+) (transport activity) were measured in mononuclear leucocytes from 37 untreated hypertensive patients and 85 normotensive subjects. Ouabain binding was lower and transport activity per binding site higher in the hypertensive patients before incubation (p less than 0.001), but both variables were normal after incubation for 72 hours with fetal calf serum. To determine whether a circulating inhibitor of sodium pumps was present in patients with hypertension ouabain binding and 86Rb+ uptake were measured in normal leucocytes before and after incubation for 72 hours with serum from 13 untreated hypertensive patients and 18 normotensive subjects. Ouabain binding was lower after incubation of cells with serum from hypertensive patients than after incubation with normal serum both before (p less than 0.01) and after (p less than 0.001) dialysis of the serum. The results suggest that in hypertension a circulating serum inhibitor of the sodium pump causes a chronic but reversible reduction in the number of pumps.

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