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/ mice kidney
Second Department of Internal Medicine, Tokyo Medical and Dental University, Tokyo 113-8519, Japan
The CLC-K1 chloride channel is a kidney-specific
CLC chloride channel expressed in the thin ascending limb of Henle's
loop (tAL). Recently, we determined that Clcnk1
/ mice
show nephrogenic diabetes insipidus (NDI). To investigate the
pathogenesis of impaired urinary concentrating ability, we analyzed
renal functions of Clcnk1/ mice in more detail. The
osmolar clearance-to-creatinine clearance ratio was not significantly
different between Clcnk1+/ and Clcnk1+/+ mice.
Fractional excretion of sodium, chloride, and urea was also not
significantly affected in Clcnk1/ mice. These results
indicate that the polyuria observed in Clcnk1/ mice was
water diuresis and not osmotic diuresis. The papillary osmolarity
in Clcnk1/ mice was significantly lower than that in Clcnk1+/+ mice under a hydrated condition, and it did not
increase even after water deprivation. Sodium and chloride contents in the inner medulla in Clcnk1/ mice were at about one-half
the levels observed in Clcnk1+/+ mice. Furthermore, the
accumulation of urea was also impaired in Clcnk1/ mice,
suggesting that the overall countercurrent system was impaired by a
defect of its single component, chloride transport in the tAL. The
aldose reductase mRNA abundance in Clcnk1/ mice was
decreased, further evincing that inner medullary tonicity is decreased
in Clcnk1/ mice. We concluded that NDI in
Clcnk1/ mice resulted from an impairment in the
generation of inner medullary hypertonicity by a dysfunction of the
countercurrent systems.
chloride channel; knockout mouse; countercurrent system; osmolytes; aquaporin-2 water channel
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