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

  • You, Ju-Hee (Departments of Pediatrics, Gwangju Christian Hospital) ;
  • Lee, Sung-Su (Departments of Physiology, Chonnam National University Medical School) ;
  • Bae, Eun-Hui (Departments of Internal Medicine, Chonnam National University Medical School) ;
  • Ma, Seong-Kwon (Departments of Internal Medicine, Chonnam National University Medical School) ;
  • Kim, Soo-Wan (Departments of Internal Medicine, Chonnam National University Medical School) ;
  • Lee, Jong-Un (Departments of Physiology, Chonnam National University Medical School)
  • 발행 : 2006.08.30

초록

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 ($250{\sim}300\;g$ 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.

키워드

참고문헌

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