Effects of manipulation of sodium balance on erythrocyte sodium transport.

The effects of changing sodium balance on blood pressure (BP) and erythrocyte sodium transport were investigated in normotensive first-degree relatives of hypertensive patients and control subjects randomised to receive low and high salt diets for two weeks, separated by a two week washout period. Changing from high to low salt intake produced a significant fall in standing diastolic pressure (DBP) in control subjects but not in the offspring of hypertensive patients. In both groups erythrocyte sodium efflux was not changed significantly by either manoeuvre, but the relatives had a significantly higher ouabain insensitive sodium efflux rate constant on both the low and the high salt diet compared to the controls (P less than 0.05). These results are not in keeping with the hypothesis which suggests the release of a humoral sodium pump inhibitor in response to sodium loading but lend support to the view that there is a disturbance of membrane permeability to sodium in subjects genetically prone to hypertension.

Effects of changes in sodium balance on leucocyte sodium transport: qualitative differences in normotensive offspring of hypertensives and matched controls.

To investigate the effects of changes in sodium balance on blood pressure and leucocyte sodium transport, normotensive first-degree relatives of hypertensive patients and control subjects were randomized to receive low- and high-salt diets for 2 weeks, separated by a wash-out period of 2 weeks. High-salt intake failed to alter blood pressure, whereas the low-salt diet produced significant falls in standing pressures in both groups. In the control subjects leucocyte sodium efflux was not changed by either manoeuvre, but in the relatives low-salt diet stimulated ouabain-insensitive sodium efflux rate constant. There was a significant qualitative difference in the pattern of response of total efflux rate constant to the two dietary periods between the two groups of subjects. These data are not compatible with the release of a humoral sodium pump inhibitor in response to sodium-induced volume expansion, and lend support to a disturbance of membrane permeability to sodium in subjects genetically prone to hypertension.