title: Prostanoids in renal failure induced by converting enzyme inhibition in sodium-depleted rats.
abstract: Clearances of inulin (CIn) and p-aminohippurate (CPAH) were measured in four groups of rats before and after intravenous administration of acetylsalicylic 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, CIn and CPAH were similar to controls but decreased significantly with ASA. In Na-depleted, captopril-treated rats, CPAH was slightly decreased, but CIn was significantly reduced (P less than 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), F2 alpha (PGF2 alpha), and thromboxane B2 (TxB2) was measured in isolated glomeruli, cortical tubule suspensions, and medullary and papillary slices. Captopril increased PGE2 production by glomeruli and PGF2 alpha 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.
authors.affiliation: Department of Nephrology, Meir Hospital, Kfar Saba, Israel.
authors.forename: E
authors.initials: E
authors.lastname: Podjarny
authors.forename: M
authors.initials: M
authors.lastname: Rathaus
authors.forename: A
authors.initials: A
authors.lastname: Pomeranz
authors.forename: J
authors.initials: J
authors.lastname: Shapira
authors.forename: H
authors.initials: H
authors.lastname: Magen
authors.forename: N
authors.initials: N
authors.lastname: Kariv
authors.forename: J
authors.initials: J
authors.lastname: Bernheim
mesh_terms: D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure; D015237:Dinoprost; D015232:Dinoprostone; D005260:Female; D066298:In Vitro Techniques; D007444:Inulin / Q000378:metabolism; D007668:Kidney / Q000378:metabolism; D011458:Prostaglandins E / Q000096:biosynthesis*; D011460:Prostaglandins F / Q000096:biosynthesis*; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000172:deficiency* / Q000378:metabolism; D013929:Thromboxane B2 / Q000096:biosynthesis*; D010130:p-Aminohippuric Acid / Q000378:metabolism
chemical_list: D000806:Angiotensin-Converting Enzyme Inhibitors; D011458:Prostaglandins E; D011460:Prostaglandins F; D013929:Thromboxane B2; D007444:Inulin; D012964:Sodium; D015237:Dinoprost; D015232:Dinoprostone; D010130:p-Aminohippuric Acid