Decreased Expression of Na+/K+-ATPase, NHE3, NBC1, AQP1 and OAT in Gentamicin-induced Nephropathy.
10.4196/kjpp.2008.12.6.331
- Author:
Woo Kyun BAE
1
;
Jong Un LEE
;
Jeong Woo PARK
;
Eun Hui BAE
;
Seong Kwon MA
;
Suhn Hee KIM
;
Soo Wan KIM
Author Information
1. Department of Internal Medicine, Chonnam National University Medical School, Gwangju 501-757, Korea. skimw@chonnam.ac.kr
- Publication Type:Original Article
- Keywords:
Gentamicin;
Sodium transporters;
Aquaporin-1;
Organic anion transporters
- MeSH:
Animals;
Avena;
Creatinine;
Gentamicins;
Humans;
Immunoblotting;
Immunohistochemistry;
Kidney;
Male;
Organic Anion Transporters;
Osmolar Concentration;
Plasma;
Rats;
RNA, Messenger;
Sodium;
Water
- From:The Korean Journal of Physiology and Pharmacology
2008;12(6):331-336
- CountryRepublic of Korea
- Language:English
-
Abstract:
The present study was aimed to determine whether there is an altered regulation of tubular transporters in gentamicin-induced nephropathy. Sprague-Dawley male rats (200~250 g) were subcutaneously injected with gentamicin (100 mg/kg per day) for 7 days, and the expression of tubular transporters was determined by immunoblotting and immunohistochemistry. The mRNA and protein expression of OAT was also determined. Gentamicin-treated rats exhibited significantly decreased creatinine clearance along with increased plasma creatinine levels. Accordingly, the fractional excretion of sodium increased. Urine volume was increased, while urine osmolality and free water reabsorption were decreased. Immunoblotting and immunohistochemistry revealed decreased expression of Na+/K+-ATPase, NHE3, NBC1, and AQP1 in the kidney of gentamicin-treated rats. The expression of OAT1 and OAT3 was also decreased. Gentamicin-induced nephropathy may at least in part be causally related with a decreased expression of Na+/K+-ATPase, NHE3, NBC1, AQP1 and OAT.
