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Urea-selective concentrating defect in transgenic mice lacking urea transporter UT-B
Baoxue Yang1, Lise Bankir, Annemarie Gillespie
1Department of Medicine, Cardiovascular Research Institute, University of California, San Francisco, California 94143-0521, USA. byang@itsa.ucsf.edu
The Journal of Biological Chemistry
|January 17, 2002
Summary
Mice lacking the urea transporter UT-B exhibit impaired urea reabsorption, leading to a "urea-selective" urinary concentrating defect. These UT-B knockout mice reveal the transporter's crucial role in kidney function and urea balance.
Area of Science:
- Nephrology
- Molecular Biology
- Physiology
Background:
- Urea transporter UT-B is a key protein involved in urea transport in erythrocytes and kidney-descending vasa recta.
- Understanding UT-B's function is crucial for comprehending urea homeostasis and urinary concentrating mechanisms.
Purpose of the Study:
- To investigate the physiological role of urea transporter UT-B in vivo.
- To characterize the urinary concentrating ability and urea handling in UT-B knockout mice.
Main Methods:
- Isolation of mouse UT-B cDNA and generation of UT-B knockout mice via targeted gene deletion.
- Assessment of urea permeability in erythrocytes.
- Measurement of urine output, osmolality, and urea concentrations in knockout and wild-type mice.
- Analysis of urea and salt concentrations in renal inner medullas.
Main Results:
- UT-B knockout mice showed a 45-fold decrease in erythrocyte urea permeability.
- UT-B deficient mice exhibited increased daily urine output and significantly lower urine osmolality, even after water deprivation.
- These mice presented with higher plasma urea but lower urine urea concentrations, resulting in a reduced urine/plasma urea ratio, indicating impaired urea concentration.
Conclusions:
- UT-B deficiency causes a specific defect in the kidney's ability to concentrate urea, distinct from salt concentration.
- The generated UT-B knockout mice are valuable tools for studying urea transport in both renal and extrarenal tissues expressing UT-B.