Abstract
The purpose of the present study is to clarify the role of intracellular sodium concentration and the autonomic nervous system in the maintenance of blood pressure, and to examine genetic effects on these systems in young normotensives. First, the effects of sodium chloride intake on blood pressure and erythrocyte sodium concentration were examined in young normotensive men. The change in dietary sodium chloride from 50mmol/day to 340mmol/day induced no significant change in blood pressure or erythrocyte sodium concentration regardless of a family history of hypertension. The relationship between intraerythrocytic sodium concentration and blood pressure under pharmacological autonomic blockade was examined in normotensive subjects with and without a family history of hypertension under free sodium intake. After total autonomic blockade with atropine, propranolol and phentolamine, mean blood pressure did not change in normotensive subjects without a family history of hypertension (81.0±8.6 to 82.8±7.9mmHg) but increased in normotensive subjects with a family history of hypertension (84.8±9.9 to 91.6±8.3mmHg, p<0.01). The difference in mean blood pressure between the two groups was significant only after autonomic blockade (p<0.05). Intraerythrocytic sodium concentration was higher in normotensive subjects with a family history of hypertension than in normotensive subjects without a family history of hypertension, but the difference was not significant. In the combined groups, intraerythrocytic sodium concentration was significantly correlated with mean blood pressure after total autonomic blockade (r=0.68, p=0.003) rather than with basal blood pressure. These results suggest that intrinsic blood pressure, excluding the effects of the autonomic nervous systems may be associated with intracellular sodium concentration and that intrinsic blood pressure increased via elevated intracellular sodium level may be compensated for by the autonomic nervous system in normotensive subjects with a hereditary predisposition to hypertension. (Hypertens Res 1994; 17: 17-22)
