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J Biol Chem, Vol. 273, Issue 8, 4296-4299, February 20, 1998
From the Departments of Medicine, Physiology, and Pediatrics,
Cardiovascular Research Institute, University of California, San
Francisco, California 94143-0521
Water channel aquaporin-1 (AQP1) is strongly
expressed in kidney in proximal tubule and descending limb of Henle
epithelia and in vasa recta endothelia. The grossly normal phenotype in human subjects deficient in AQP1 (Colton null blood group) and in AQP4
knockout mice has suggested that aquaporins (other than the
vasopressin-regulated water channel AQP2) may not be important in
mammalian physiology. We have generated transgenic mice lacking detectable AQP1 by targeted gene disruption. In kidney proximal tubule
membrane vesicles from knockout mice, osmotic water permeability was
reduced 8-fold compared with vesicles from wild-type mice. Although the
knockout mice were grossly normal in terms of survival, physical
appearance, and organ morphology, they became severely dehydrated and
lethargic after water deprivation for 36 h. Body weight decreased
by 35 ± 2%, serum osmolality increased to >500 mOsm, and
urinary osmolality (657 ± 59 mOsm) did not change from that
before water deprivation. In contrast, wild-type and heterozygous mice
remained active after water deprivation, body weight decreased by
20-22%, serum osmolality remained normal (310-330 mOsm), and urine
osmolality rose to >2500 mOsm. Urine [Na+] in
water-deprived knockout mice was <10 mM, and urine
osmolality was not increased by the V2 agonist DDAVP. The results
suggest that AQP1 knockout mice are unable to create a hypertonic
medullary interstitium by countercurrent multiplication. AQP1 is thus
required for the formation of a concentrated urine by the kidney.
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