Prostanoids in renal failure induced by converting enzyme inhibition in sodium-depleted rats

Clearances of inulin (C(in)) and p-aminohippurate (C(PAH)) were measured in four groups of rats before and after intravenous administration of acetylsalycilic acid (ASA): 1) controls, on normal Na intake, 2) captopril-treated (30 mg·kg^-1·day^-1) on normal Na intake, 3) Na depleted, and 4) Na depleted, captopril-treated. In Na-depleted animals, C(In) and C(PAH) were similar to controls but decreased significantly with ASA. In Na-depleted, captopril-treated rats, C(PAH) was slightly decreased, but C(In)( was significantly reduced (P < 0.01). Both were not affected by ASA. Urine output was unchanged and the kidneys appeared normal on histological examination. The production of prostaglandins E₂ (PGE₂), F(2α), (PGF(2α)), and thromboxane B₂ (TxB₂) was measured in isolated glomeruli, cortical tubule suspensions, and medullary and papillary slices. Captopril increased PGE₂ production by glomeruli and PGF(2α) and TxB₂ synthesis in papillary slices. Na depletion selectively enhanced the production of PGE₂ by glomeruli and papillae. In contrast, the synthesis of prostanoids was significantly decreased in captopril-treated, Na-depleted rats. These findings suggest that in this model, functional nonoliguric renal failure may be related to abnormalities of prostanoid synthesis.