Role of Volume and Prostaglandin Synthesis in the Suppression of Renin by Saline in the Rat

To evaluate the contribution of plasma volume expansion per se on acute inhibition of renin release by sodium chloride infusion, renin responses to comparable plasma volume expansion with intravenous infusions of sodium chloride, sodium bicarbonate, or albumin were studied in separate groups of sodium chloride-depleted rats. In addition, urinary prostaglandin E2 (PGE2) excretion rate was compared in the saline- and sodium bicarbonate-infused animals to evaluate the relationship between acute changes in renin release and intrarenal PGE2 synthesis. All three groups were plasma volume-expanded by approximately 55%. Plasma renin activity (PRA) decreased in response to saline (12.3 ± 1.0 to 6.7 ± 0.7 ng AI/ml/hr; P < 0.01) whereas PRA did not change with sodium bicarbonate (11.3 ± 1.4 to 10.2 ± 1.5) or albumin (9.9 ± 0.7 to 8.2 ± 1.0). The rate of PGE2 excretion was not changed by either saline (72.2 ± 13.1 to 72.3 ± 18.7 pg/min) or sodium bicarbonate infusion (70.7 ± 8.8 to 64.9 ± 7.0). These results support the hypothesis that acute suppression of PRA by infusion of saline is not dependent upon volume expansion per se. In confirmation of earlier observations, inhibition of renin release by sodium chloride was related to chloride. Finally, the results suggest that the renal tubular mechanism for inhibition of renin release by sodium chloride is not related to overall changes in renal PGE2 synthesis in the rat.