| Project/Area Number |
13671121
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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 | Kumamoto University |
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Principal Investigator |
NONOGUCHI Hiroshi Kumamoto University, Department of Nephrology, Associate Professor, 医学薬学研究科・腎臓内科, 助教授 (30218341)
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| Co-Investigator(Kenkyū-buntansha) |
TOMITA Kimio Kumamoto University, Department of Nephrology, Professor, 医学薬学研究科・腎臓内科, 教授 (40114772)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2002: ¥1,700,000 (Direct Cost: ¥1,700,000)
Fiscal Year 2001: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | antidiuretic hormone / V1a receptor / V2 receptor / aquaporin 2 / trafficking / metabolic acidosis / 転写活性 / Vla受容体 / 慢性腎不全 / 集合尿細管 / RT-PCR |
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| Research Abstract |
We first investigated urinary excretion of aquaporin 2 (AQP2) using Western blot analysis. However, AQP2 was not detectable in the urine. We have been still trying to detect urinary excretion of AQP2 by increasing the sensitivity of Western blot analysis. Urinary excretion of AQP2 was also examined in rats with metabolic acidosis. Urinary excretion of AQP2 was significantly decreased in metabolic acidosis. However, the expressions of AQP2 mRNA and protein in outer medullary collecting ducts were increased. Differential centrifugation revealed that AQP2 expression was decreased in membrane-rich fraction but increased in intracellular vesicle-rich fraction. These data suggest that trafficking of AQP2 from intracellular vesicles to apical membrane is inhibited in metabolic acidosis. The precise mechanisms of the disturbance has to be examined further.
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