Korean J Physiol Pharmacol.  2006 Aug;10(4):213-216.

Blunted Indomethacin-Induced Downregulation of Aquaporins by Nitric Oxide Synthesis Inhibition in Rats

  • 1Department of Physiology, Chonnam National University Medical School, Gwangju, Korea. julee@jnu.ac.kr
  • 2Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea.
  • 3Department of Pediatrics, Gwangju Christian Hospital, Gwangju, Korea.


The present study was aimed to determine whether nitric oxide (NO) plays a role in the regulation of aquaporin (AQP) channels in the kidney. Male Brattleboro rats (250~300 g body weight) were used. The experimental group was treated with N(G)-nitro-L-arginine methyl ester (L-NAME, 100 mg/L drinking water) for 1 week, and cotreated with indomethacin (5 mg/kg, twice a day, i.p.) for the last two days. Control groups were treated with either L-NAME for 1 week, indomethacin for 2 days, or without any drug treatment. The abundance of AQP1, AQP2 and AQP3 proteins in the kidney was determined by Western blot analysis. Indomethacin downregulated AQP channels, whereas L-NAME by itself showed no significant effects on them. The indomethacin-induced downregulation of AQP2 and AQP3 was significantly blunted in L-NAME-treated rats, while that of AQP1 was not affected. These results suggest that endogenous NO, when stimulated, may downregulate AQP channels that are specifically regulated by AVP/cAMP pathway in the kidney.


AQP water channels; Indomethacin; NG-nitro-L-arginine methyl ester
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