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      Post-Obstruction Diuresis: Influence of Renal Prostaglandins


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          The possible role of altered renal prostaglandin metabolism in the generation of post-obstruction diuresis (POD) was examined in 16 adult male Sprague-Dawley rats. Inhibition of cyclooxygenase by the administration of a combination of two nonsteroidal anti-inflammatory drugs (NSAID), meclofenamate and indomethacin in 8 of these rats exaggerated, rather than lowered the degree of natriuresis and diuresis that followed the release 24 h after bilateral ureteral ligation. Urine osmolarity was similar in the two groups of rats treated with the NSAID and vehicle. The results suggest an enhanced synthesis of renal vasoconstrictor and antidiuretic prostaglandins (thromboxane A<sub>2</sub> or PGF<sub>2α</sub>) during bilateral ureteral ligation. NSAIDs such as aspirin, indomethacin, meclofenamate and others may promote POD by blocking this prostaglandin pathway while promoting the cytochrome P450 monooxygenase pathway which may produce vasodilator, diuretic and natriuretic paracrine hormones. Additionally, inhibition of prostaglandin synthesis may have enhanced post-obstruction diuresis in the present studies by allowing a greater volume expansion during obstruction, as indicated by a reduced hematocrit in the rats that were pretreated with NSAID.

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          Author and article information

          S. Karger AG
          11 December 2008
          : 60
          : 3
          : 281-285
          Department of Physiology and Pharmacology, and Department of Medicine, University of South Dakota, School of Medicine, Vermillion, S. Dak., USA
          186766 Nephron 1992;60:281–285
          © 1992 S. Karger AG, Basel

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          : 21 June 1991
          Page count
          Pages: 5
          Original Paper

          Cardiovascular Medicine,Nephrology
          Diuresis,Prostaglandins,Ureteral obstruction,Natriuresis,Meclofenamate,Indomethacin,Kidney function,Hydronephrosis,Anti-inflammatory drugs,Bilateral ureteral obstruction


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