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Papers In Press, published online ahead of print January 15, 2002
Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA 94143-0521
Corresponding Author: verkman{at}itsa.ucsf.edu
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 wildtype littermates. Urea permeability was 45-fold lower in erythrocytes from knockout than wildtype 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 vs. 2056 ± 83 mosm/kgH2O, SE, p<0.001). After 24 h water deprivation, Uosm (in mosm/kgH2O) was 2403 ± 38 in UT-B null mice and 3438 ± 98 in wildtype mice (p<0.001). Plasma urea concentration (Purea) was 30 % higher and urine urea concentration (Uurea) 35 % lower in knockout than in wildtype mice, resulting in much lower Uurea/Purea ratio (61 ± 5 vs. 124 ± 9, p<0.001). Thus the capacity to concentrate urea in the urine is more severely impaired than that to concentrate other solutes. Together with data showing a disproportionate reduction in the concentration of urea compared to 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.
J. Biol. Chem, 10.1074/jbc.M200207200
Submitted on January 8, 2002
Revised on January 12, 2002
Accepted on January 14, 2002
Urea-selective urinary concentrating defect in transgenic mice lacking urea transporter UT-B
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