| Project/Area Number |
21591064
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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 | Hyogo Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
NAKANISHI Takeshi 兵庫医科大学, 医学部, 教授 (70217769)
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| Co-Investigator(Renkei-kenkyūsha) |
TOMITA Kimio 熊本大学, 大学院・生命科学研究部, 教授 (40114772)
KAWAHARA Kastumasa 北里大学, 医学部, 教授 (70134525)
NAKAYAMA Yushi 熊本大学, 大学院・生命科学研究部, 講師 (00363531)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Keywords | 水・電解質代謝学 / 抗利尿ホルモン / レニン・アンジオテンシン・アルドステロン系 / ミネラルコルチコイド受容体 / 細胞質核内輸送 / V1a受容体 / アルドステロン / 腎尿細管性アシドーシス / ミネラロコルチコイド受容体 / 細胞質・核輸送 / 核内受容体 / 介在細胞 / V2受容体 / ノックダウン / 抗体利尿ホルモン / ノックアウトマウス / トランスジェニックラット / H-ATPase |
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| Research Abstract |
We reported that vasopressin V1a receptor deficient mice show type 4 renal tubular acidosis, which is characterized by reduced renal function, metabolic acidosis and hyperkalemia. Since the colleting ducts are the main cite of acid secretion by the kidney, we established a new cell line of the intercalated cells(IN-IC cells) from SV40 large T antigen Tg rats. Using these cells, we also found that vasopressin V1a receptor is required for nucleocytoplasmic transport of mineralocorticoid receptor by aldosterone in the intercalated cells. In conclusion, vasopressin V1a receptor is essential for acid-base regulation by aldosterone in intercalated cells. These data suggest the possibility of clinical use of vasopressin V1a receptor antagonist as an aldosterone antagonist.
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