Analysis of urine concentrating mechanisms using the CLC-K1 null mice.
| Project/Area Number |
12671028
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | TOKYO MEDEICAL AND DENTAL UNIVERSITY |
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Principal Investigator |
UCHIDA Shinichi TOKYO MEDEICAL & DENTAL UNIVERSITY, Associate Professor, 医学部・附属病院, 講師 (50262184)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2000: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | chloride Channel / counter current system / knockout mice / 尿濃縮 |
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| Research Abstract |
CLC-K1 is a chloride channel responsible for transepithelial chloride transport in the thin ascending limb of Henle's loop in the kidney. This chloride had been postulated to constitute a countercurrent system for urinary concentration mechanism in the inner medulla of the kidney. We generated the CLC-K1 knockout mice and found that the mice showed nephrogenic diabetes inspidus (NDI). However, exact mechanisms of NDI remained to be determined. In this study, we measured tissue osmolarity and electrolytes contents in the inner medulla of wild-type and the knockout mice. We found that the defect of a chloride transport system alone affected the overall accumulation of osmolar substances including urea and Na. This confirmed that a countercurrent system did not work without its single component, and verified for the first time that the countersystem really works in vivo.
We also described the developmental changes of CLC-K1 expression in neonatal kidney. Moreover, using the CLC-K1 mice, we could precisely determine its closely related chloride channel, CLC-K2, in the mouse kidney.
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Report
(3 results)
Research Products
(18 results)
