SALT SENSITIVITY AND CELL-PERMEABILITY

We have recently shown that changes in blood sodium concentration within the limited range of +/- 15 mmol/l induce changes in blood pressure which are directly related to intracellular sodium concentration and inversely related to the transmembrane sodium gradient. It followed from this that the blood pressure response to an incremental change in blood sodium concentration induced by an intraperitoneal salt load should be a function of the rate of accumulation of cell sodium. This was tested in rats treated with deoxycorticosterone acetate (DOCA)-saline for 3 days since at this time cell permeability to sodium is known to be increased. The rise of cell sodium when blood sodium concentration, measured 30 min after loading, ranged from 140-160 mmol/l, was significantly increased in treated animals (0.14 versus 0.21 mmol/kg dry weight for each 1 mmol/l rise in extracellular sodium concentration) and the rise in blood pressure was correspondingly greater (0.81 versus 1.43 mmHg for a 1 mmol/l rise in extracellular sodium concentration). The increased accumulation of cell sodium was not accompanied by a similar increase in water, so that the rise in intracellular sodium concentration was also exaggerated. Prior uninephrectomy slowed the excretion of the salt load sufficiently to exaggerate the rise of blood sodium concentration in response to a given load. The osmotic effects of intraperitoneal high sodium or high sucrose were both equally reduced, indicating that the increased permeability induced by DOCA is not specific for sodium but affects non-electrolytes as well; thus, it probably involves the phospholipid matrix.