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Renal Expression of Aquaporins in Liver Cirrhosis Induced by Chronic Common Bile Duct Ligation in Rats

PATRICIA FERNÁNDEZ-LLAMA^*, RACHEL TURNER^*, GERALD DIBONA and MARK A. KNEPPER^*

^* Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland
Department of Internal Medicine, University of Iowa College of Medicine and Veterans Administration Medical Center, Iowa City, Iowa.

Correspondence to Dr. Mark A. Knepper, National Institutes of Health, Building 10, Room 6N260, 10 Center Drive, MSC 1603, Bethesda, MD 20892-1603. Phone: 301-496-3064; Fax: 301-402-1443; E-mail: knep{at}helix.nih.gov

Abstract

Abstract. Semiquantitative immunoblotting was used to investigate the expression levels of the four major renal aquaporins, the Na-K-2Cl cotransporter of the thick ascending limb, the type 3 Na-H exchanger, and the Na-K-ATPase in kidneys from rats with cirrhosis secondary to common bile duct ligation (CBDL). These rats had significant water retention and hyponatremia. In contrast to models of cirrhosis induced by carbon tetrachloride, aquaporin-2 expression in CBDL-induced cirrhosis was decreased. Thus, these results show that in the setting of extracellular fluid volume expansion, excessive water retention with hyponatremia can occur in the absence of increases in aquaporin-2 abundance. In addition, the expression levels of the two basolateral collecting duct aquaporins (aquaporin-3 and -4) were decreased in CBDL rats relative to sham-operated control rats. Similarly, the Na-K-2Cl cotransporter of the thick ascending limb and the type 3 Na-H exchanger showed decreases in expression. In contrast, the expression levels of aquaporin-1 and the 1 subunit of the Na-K-ATPase were not decreased. Thus, dysregulation of multiple water channels and ion transporters may play a role in water balance abnormalities associated with CBDL-induced cirrhosis in rats.

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