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      Transient Body Fluid Accumulation and Enhanced NKCC2 Expression in Gerbils with Brain Infarction

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          Background: Enhanced expression of a kidney-specific sodium co-transporter (NKCC2: Na-K-2Cl co-transporter) in the thick ascending limb of Henle has been identified in rat models of congestive heart failure and liver cirrhosis, suggesting that high NKCC2 expression underlies edema formation. An increased abundance of NKCC2, however, has also been noted in rats with the syndrome of inappropriate secretion of antidiuretic hormone; hyponatremia without edema. In the present study, we examined NKCC2 expression in non-edematous disease, such as a brain infarction, and investigated the physiological and/or pathological characterization of NKCC2 expression. Methods:We initially examined NKCC2 expression in an animal model of brain infarction. Mongolian gerbils (around 60 g body weight) underwent bilateral clamping of the common carotid arteries for 5 min for the induction of brain infarction. NKCC2 and apical water channel (AQP2) protein levels in the collecting duct were examined by Western blotting in kidney tissues 2, 7, and 14 days after the brain infarction. Gerbils with brain infarction were then fed either a normal low-sodium diet (0.3 g/kg/day) or a high-sodium diet (3.0 g/kg/day), and body weight, urine volume and urinary osmolality were examined daily. Blood parameters were measured on day 14 after the brain infarction. Results: Histochemical examination of the brain confirmed the presence of brain infarction, as manifested by altered cresyl violet staining in the hippocampus. Protein levels of NKCC2 were significantly increased in gerbils with brain infarction on days 2 and 7 after brain infarction, whereas AQP2 protein signals remained unaltered. However, the increased NKCC2 intensity disappeared on day 14. Body weight gain was slightly, but significantly greater in gerbils with brain infarction than in sham-operated gerbils up to 7 days after the brain infarction. The high-sodium diet resulted in significant urinary concentration and enhanced weight gain in infarcted gerbils. Conclusion: We noted increased NKCC2 abundance in non-edematous disease, which enhanced body fluid accumulation, likely via the sodium loading-dependent concentration of the urine. These results suggest that the physiological process of edema formation is based on specific NKCC2 expression. The transient duration of these findings in the present animal model suggests two different characteristics of specific NKCC2 expression, an immediate, transient appearance as a common response in serious conditions and more chronic expression that leads to edema formation.

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          Most cited references 18

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          Cloning and expression of apical membrane water channel of rat kidney collecting tubule.

          Concentrating urine is mandatory for most mammals to prevent water loss from the body. Concentrated urine is produced in response to vasopressin by the transepithelial recovery of water from the lumen of the kidney collecting tubule through highly water-permeable membranes. In this nephron segment, vasopressin regulates water permeability by endo- and exocytosis of water channels from or to the apical membrane. CHIP28 is a water channel in red blood cells and the kidney proximal tubule, but it is not expressed in the collecting tubule. Here we report the cloning of the complementary DNA for WCH-CD, a water channel of the apical membrane of the kidney collecting tubule. WCH-CD is 42% identical in amino-acid sequence to CHIP28. WCH-CD transcripts are detected only in the collecting tubule of the kidney. Immunohistochemically, WCH-CD is localized to the apical region of the kidney collecting tubule cells. Expression of WCH-CD in Xenopus oocytes markedly increases osmotic water permeability. The functional expression and the limited localization of WCH-CD to the apical region of the kidney collecting tubule suggest that WCH-CD is the vasopressin-regulated water channel.
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            The syndrome of inappropriate secretion of antidiuretic hormone.

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              Cellular and subcellular immunolocalization of vasopressin-regulated water channel in rat kidney.


                Author and article information

                Nephron Physiol
                Nephron Physiology
                S. Karger AG
                April 2006
                11 April 2006
                : 103
                : 1
                : p25-p32
                Divisions of aMolecular Medicine, bAnesthesiology and Perioperative Medicine, and cAdvanced Surgical Science and Technology, Tohoku University School of Medicine, Sendai, dTaisyo Pharmaceutical Company, Tokyo, eDepartment of Kampo Pharmaceutical Sciences, Nihon Pharmaceutical University, Saitama, and fDepartment of Homeostasis Medicine and Nephrology, Tokyo Medical and Dental University, Tokyo, Japan
                90220 Nephron Physiol 2006;103:p25–p32
                © 2006 S. Karger AG, Basel

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                Page count
                Figures: 4, Tables: 1, References: 30, Pages: 1
                Self URI (application/pdf): https://www.karger.com/Article/Pdf/90220
                Original Paper

                Cardiovascular Medicine, Nephrology

                Edema, AQP2, Urinary concentration, High-sodium diet


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