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Am J Physiol Renal Physiol 278: F75-F82, 2000;
0363-6127/00 $5.00
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Vol. 278, Issue 1, F75-F82, January 2000

Abnormal water metabolism in mice lacking the type 1A receptor for ANG II

Michael I. Oliverio1, Marielle Delnomdedieu2, Christopher F. Best1, Ping Li3, Mariana Morris3, Michael F. Callahan4, G. Allan Johnson2, Oliver Smithies5, and Thomas M. Coffman1

1 Department of Medicine, 2 Center for In Vivo Microscopy, Duke University, and Veterans Affairs Medical Centers, Durham 27710; 4 Departments of Pharmacology and Physiology, Bowman Gray School of Medicine, Winston-Salem 27257; 5 Department of Pathology, University of North Carolina, Chapel Hill, North Carolina 27599; and 3 Department of Pharmacology, Wright State University, Dayton, Ohio 45401

Mice lacking AT1A receptors for ANG II have a defect in urinary concentration manifested by an inability to increase urinary osmolality to levels seen in controls after thirsting. This defect results in extreme serum hypertonicity during water deprivation. In the basal state, plasma vasopressin levels are similar in wild-type controls and Agtr1a -/- mice. Plasma vasopressin levels increase normally in the AT1A receptor-deficient mice after 24 h of water deprivation, suggesting that the defect in urine concentration is intrinsic to the kidney. Using magnetic resonance microscopy, we find that the absence of AT1A receptors is associated with a modest reduction in the distance from the kidney surface to the tip of the papilla. However, this structural abnormality seems to play little role in the urinary concentrating defect in Agtr1a -/- mice since the impairment is largely reproduced in wild-type mice by treatment with an AT1-receptor antagonist. These studies demonstrate a critical role for the AT1A receptor in maintaining inner medullary structures in the kidney and in regulating renal water excretion.

gene targeting; urinary concentration; magnetic resonance microscopy; papilla; vasopressin


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