Blunted Indomethacin-Induced Downregulation of Aquaporins by Nitric Oxide Synthesis Inhibition in Rats.
- Author:
Ju Hee YOU
1
;
Sungsu LEE
;
Eun Hui BAE
;
Seong Kwon MA
;
Soo Wan KIM
;
Jong Un LEE
Author Information
1. Department of Physiology, Chonnam National University Medical School, Gwangju, Korea. julee@jnu.ac.kr
- Publication Type:Original Article
- Keywords:
AQP water channels;
Indomethacin;
NG-nitro-L-arginine methyl ester
- MeSH:
Animals;
Aquaporin 3;
Aquaporins*;
Blotting, Western;
Down-Regulation*;
Drinking;
Humans;
Indomethacin;
Kidney;
Male;
NG-Nitroarginine Methyl Ester;
Nitric Oxide*;
Rats*;
Rats, Brattleboro
- From:The Korean Journal of Physiology and Pharmacology
2006;10(4):213-216
- CountryRepublic of Korea
- Language:English
-
Abstract:
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.
