Article
Severely impaired urine-concentrating ability in mice lacking the CLC-K1 chloride channel.
Experimental nephrology - 1 Jan 2000
Uchida S, Marumo F
Abstract excerpt
To analyze the physiological functions of CLC-K1 in vivo, we generated mice lacking CLC-K1 by targeted gene disruption. Homozygous mutant Clcnk1-/- mice produced approximately 5 times more urine than Clcnk1+/- and Clcnk1+/+ mice. After 24-hour water deprivation, Clcnk1-/- mice became severely dehydrated and lethargic. Intraperitoneal injection of the V2 agonist, deamino-Cys(1), D-Arg(8) vasopressin, induced an...
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