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      Urinary Excretion and Glomerular Synthesis of Prostaglandin E 2 and Prostaglandin F in Cirrhotic, Non-Ascitic Rats: The Effects of Sodium Overload

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          Abstract

          The urinary excretion of aldosterone, kallikrein and prostaglandin E<sub>2</sub> (PGE<sub>2</sub>) was studied in sodium-retaining (RC) and nonretaining (NRC), nonascitic cirrhotic rats, under basal conditions and after an oral sodium load (5 mmol). The glomerular synthesis of PGE<sub>2</sub> was measured in RC rats under the same conditions. Both groups of cirrhotic animals showed a decreased urinary excretion of PGE<sub>2</sub>. Isolated glomeruli of RC rats produced less PGE<sub>2 </sub>than those of the control animals, both under basal conditions and after the sodium load. The NRC group was the only one able to increase the urinary excretion of kallikrein in response to the sodium load. These findings could contribute to explain the early physiopathological events of hepatic cirrhosis.

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          Author and article information

          Journal
          NEF
          Nephron
          10.1159/issn.1660-8151
          Nephron
          S. Karger AG
          1660-8151
          2235-3186
          1988
          1988
          09 December 2008
          : 49
          : 4
          : 322-327
          Affiliations
          Laboratory of Renal Physiopathology, Department of Nephrology, Fundación Jiménez Díaz, Madrid, Spain
          Article
          185084 Nephron 1988;49:322–327
          10.1159/000185084
          3166114
          © 1988 S. Karger AG, Basel

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          Page count
          Pages: 6
          Categories
          Original Paper

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