Blockade of Nitric Oxide Synthesis Further Diminishes Aquaporin Water Channels in Rat Kidney Subjected to Ischemia/reperfusion Injury.
- Author:
Seong Kwon MA
1
;
Yoon Wha OH
;
Choonsoon PARK
;
Youn Kyoung LEE
;
Soo Wan KIM
;
Nam Ho KIM
;
Ki Chul CHOI
;
JongUn LEE
Author Information
1. Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea. drmsk@hanmail.net
- Publication Type:Original Article
- Keywords:
Nitric oxide;
Ischemia;
Reperfusion;
Aquaporin
- MeSH:
Animals;
Aquaporins*;
Blotting, Western;
Constriction;
Ischemia;
Kidney*;
NG-Nitroarginine Methyl Ester;
Nitric Oxide*;
Rats*;
Renal Artery;
Reperfusion
- From:Korean Journal of Nephrology
2006;25(1):7-12
- CountryRepublic of Korea
- Language:English
-
Abstract:
BACKGOUND: The present study examined whether a blockade of nitric oxide (NO) synthesis affects the regulation of aquaporin (AQP) water channels in rats subjected to renal ischemia/reperfusion (I/R). METHODS: Renal I/R was experimentally induced by clamping the left renal artery for 60 minutes in rats. The rats were kept for 7 days thereafter, during which they were supplied with tap water containing NG-nitro-L-arginine methyl ester (L-NAME, 100 mg/L). The expression of AQP1-3 was determined in the kidney by Western blot analysis. RESULTS: In renal I/R injury, the expression of AQP2 was significantly decreased. The treatment with L-NAME further diminished the expression of AQP2. Although the expression of either AQP1 or AQP3 was not significantly altered in the kidney subjected to I/R, it was also significantly decreased by the treatment with L-NAME. CONCLUSION: It is suggested that endogenous NO system should play a role in the regulation of AQP water channels in rat kidney subjected to I/R injury.
