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

E. Podjarny, M. Rathaus, A. Pomeranz, J. Shapira, H. Magen, N. Kariv, J. Bernheim

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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.

Original languageEnglish
Pages (from-to)F358-F363
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Issue number3 (23/3)
StatePublished - 1988
Externally publishedYes


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