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This Article Full Text Full Text (PDF) All Versions of this Article: 294/1/F272    most recent 00352.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (3) Citing Articles via Google Scholar Google Scholar Articles by Bae, E. H. Articles by Kim, S. W. Search for Related Content PubMed PubMed Citation Articles by Bae, E. H. Articles by Kim, S. W.

Effects of -lipoic acid on ischemia-reperfusion-induced renal dysfunction in rats

Departments of ¹Internal Medicine and ²Physiology and ³Cardiovascular Research Institute, Chonnam National University, Gwangju; ⁴The Water and Salt Research Center, University of Aarhus, Aarhus C, Denmark; and ⁵Department of Physiology, Chonbuk National University Medical School, Jeonju, Korea

Submitted 28 July 2007 ; accepted in final form 12 November 2007

We investigated whether -lipoic acid (-LA), an antioxidant, attenuates the ischemia-reperfusion (I/R)-induced dysregulation of these transporters. Both renal pedicles of male Sprague-Dawley rats were clamped for 40 min. -LA (80 mg/kg) was administered intraperitoneally before and immediately after induction of ischemia. After 2 days, the expression of aquaporins (AQPs), sodium transporters, and nitric oxide synthases (NOS) was determined in the kidney by immunoblotting and immunohistochemistry. The expression of endothelin-1 (ET-1) mRNA was determined by real-time PCR. Activities of adenylyl cyclase and guanylyl cyclase were measured by stimulated generation of cAMP and cGMP, respectively. The expression of AQP1–3 as well as that of the ₁-subunit of Na-K-ATPase, type 3 Na/H exchanger, Na-K-2Cl cotransporter, and Na-Cl cotransporter was markedly decreased in response to I/R. The expression of type VI adenylyl cyclase was decreased in I/R-injured rats, which was counteracted by the treatment of -LA. AVP-stimulated cAMP generation was blunted in I/R rats and was then ameliorated by -LA treatment. -LA treatment attenuated the downregulation of AQPs and sodium transporters. The expression of endothelial NOS was decreased in I/R rats, which was prevented by -LA. The cGMP generation in response to sodium nitroprusside was blunted in I/R rats, which was also significantly prevented by -LA. The mRNA expression of ET-1 was increased, which was recovered to the control level by -LA treatment. In conclusion, -LA treatment prevents I/R-induced dysregulation of AQPs and sodium transporters in the kidney, possibly through preserving normal activities of local AVP/cAMP, nitric oxide/cGMP, and ET systems.

I/R injury; aquaporins; sodium transporters; nitric oxide; endothelin

This article has been cited by other articles:

				E. H. Bae, J. Lee, S. K. Ma, I. J. Kim, J. Frokiaer, S. Nielsen, S. Y. Kim, and S. W. Kim {alpha}-Lipoic acid prevents cisplatin-induced acute kidney injury in rats Nephrol. Dial. Transplant., September 1, 2009; 24(9): 2692 - 2700. [Abstract] [Full Text] [PDF]