A high sodium diet (750 mEq/kg) in subtotally nephrectomized rats led to a continuous rise in blood pressure up to a mean of 178 +/- 9 mmHg over four weeks, driven by volume expansion.
Does a high sodium diet induce hypertension and hemodynamic changes in subtotally nephrectomized rats?
In a rat model of subtotal nephrectomy, high sodium intake induces hypertension driven by fluid retention and increased osmolarity rather than renin-angiotensin system activation.
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 osmolarity, 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.
Ylitalo et al. (Wed,) conducted a other in Sodium-induced hypertension. High sodium diet vs. Sham-operated animals on high sodium supply and sham-operated controls on standard sodium diet (150 mEq/kg) was evaluated on Blood pressure. A high sodium diet (750 mEq/kg) in subtotally nephrectomized rats led to a continuous rise in blood pressure up to a mean of 178 +/- 9 mmHg over four weeks, driven by volume expansion.
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