Korean J Nephrol.  2006 Jan;25(1):7-12.

Blockade of Nitric Oxide Synthesis Further Diminishes Aquaporin Water Channels in Rat Kidney Subjected to Ischemia/reperfusion Injury

Affiliations
  • 1Department of Internal Medicine, Chonnam National University Medical School, Gwangju, Korea. drmsk@hanmail.net
  • 2Department of Physiology, Chonnam National University Medical School, Gwangju, Korea.

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.

Keyword

Nitric oxide; Ischemia; Reperfusion; Aquaporin

MeSH Terms

Animals
Aquaporins*
Blotting, Western
Constriction
Ischemia
Kidney*
NG-Nitroarginine Methyl Ester
Nitric Oxide*
Rats*
Renal Artery
Reperfusion
Aquaporins
NG-Nitroarginine Methyl Ester
Nitric Oxide
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