Abstract
Hemodynamic changes during the development of sodium–induced hypertension were investigated in male Sprague–Dawley rats after about 70% of the renal mass was removed. Throughout the four experimental weeks, subtotally nephrectomized rats on a high sodium diet (750 mEq/kg) showed a continuous rise in blood pressure up to the mean value of 178±9 mmHg. In sham–operated animals on the high sodium supply the blood pressure did not increase, as compared to sham–operated controls on the standard sodium diet (150 mEq/kg). In the hypertensive group, the primary changes were urea retention and a concomitant increase of serum osmolality, but the serum sodium concentration remained at the normal level. These changes were followed by sustained enlargement of extracellular fluid and relative intravascular volumes, together with a simultaneous increase of heart rate and blood pressure. During high sodium intake, the plasma renin activity in subtotally nephrectomized rats was suppressed to one fifth of that in sham–operated animals, but the renin substrate activity did not increase markedly.

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