Cellular mechanism relating sodium and potassium to hypertension

It was found that the higher the [Na+]i is in erythrocytes and leukocytes and the lower the Na pump activity the higher is the blood pressure level. In normotensive people the [Na+]i in blood cells was lower and the leukocyte [K+]i higher, which is in accordance with the discovery that the erythrocyte Na-K ATPase was increased which denotes the hyperfunction of the Na pump activity. These intracellular cation concentration changes were more prominent in men than in women and were more prominent in people whose both parents were hypertensive compared to those with only one parent being hypertensive. It is suspected that the inward and outward co-transport system dearrangement in the cell membrane found by us might be implicated in the appearance of compensatory hyperfunction of the Na pump activity. The humoral Na pump inhibiting factor appears to be an endogeneous digitalis-like substance which is increased in the plasma of hypertensive patients and their offsprings. This might be contributing to the inhibition of the Na pump activity during the development of hypertension. The abnormality rate of the inward co-transport (delta Na less than 0.5 mmol/l erythrocyte) in people with one or both parents being hypertensive, was 46% and 59% respectively. The difference between these percentages was, however, not statistically significant. The appearance of a double-peak in the delta Na frequency curve and the emergence of delta Na abnormality among three generations suggest that the low co-transport, which was significantly associated with hypertension, might be transmitted as a monogeneic, dominant, autosomal trait.