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Originally published In Press as doi:10.1074/jbc.M200207200 on January 15, 2002

J. Biol. Chem., Vol. 277, Issue 12, 10633-10637, March 22, 2002
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Urea-selective Concentrating Defect in Transgenic Mice Lacking Urea Transporter UT-B*

Baoxue YangDagger §, Lise BankirDagger , Annemarie Gillespie||, Charles J. Epstein||, and A. S. VerkmanDagger

From the Departments of Dagger  Medicine and Physiology and || Pediatrics, Cardiovascular Research Institute, University of California, San Francisco, California 94143-0521 and  INSERM Unit 367, Institut du Fer a Moulin, 75005 Paris, France

Urea transporter UT-B has been proposed to be the major urea transporter in erythrocytes and kidney-descending vasa recta. The mouse UT-B cDNA was isolated and encodes a 384-amino acid urea-transporting glycoprotein expressed in kidney, spleen, brain, ureter, and urinary bladder. The mouse UT-B gene was analyzed, and UT-B knockout mice were generated by targeted gene deletion of exons 3-6. The survival and growth of UT-B knockout mice were not different from wild-type littermates. Urea permeability was 45-fold lower in erythrocytes from knockout mice than from those in wild-type mice. Daily urine output was 1.5-fold greater in UT-B- deficient mice (p < 0.01), and urine osmolality (Uosm) was lower (1532 ± 71 versus 2056 ± 83 mosM/kgH2O, mean ± S.E., p < 0.001). After 24 h of water deprivation, Uosm (in mosM/kgH2O) was 2403 ± 38 in UT-B null mice and 3438 ± 98 in wild-type mice (p < 0.001). Plasma urea concentration (Purea) was 30% higher, and urine urea concentration (Uurea) was 35% lower in knockout mice than in wild-type mice, resulting in a much lower Uurea/Purea ratio (61 ± 5 versus 124 ± 9, p < 0.001). Thus, the capacity to concentrate urea in the urine is more severely impaired than the capacity to concentrate other solutes. Together with data showing a disproportionate reduction in the concentration of urea compared with salt in homogenized renal inner medullas of UT-B null mice, these data define a novel "urea-selective" urinary concentrating defect in UT-B null mice. The UT-B null mice generated for these studies should also be useful in establishing the role of facilitated urea transport in extrarenal organs expressing UT-B.

* This work was supported in part by National Institutes of Health Grants HL58198, DK35124, HL60288, and HL51854 and Grant R613 from the National Cystic Fibrosis Foundation.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EBI Data Bank with accession number(s) AF448798.

§ To whom correspondence should be addressed: Cardiovascular Research Institute, 1246 Health Sciences East Tower, University of California, San Francisco, San Francisco, CA 94143-0521. Tel.: 415-476-8530; Fax: 415-665-3847; E-mail: byang@itsa.ucsf.edu or www.ucsf.edu/verklab.

Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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