| Project/Area Number |
11670050
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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 |
General physiology
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| Research Institution | KITASATO UNIVERSITY |
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Principal Investigator |
KAWAHARA Katsumasa Kitasato Univ.School of Medicine Professor, 医学部, 教授 (70134525)
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| Co-Investigator(Kenkyū-buntansha) |
ANZAI Naohiko Kitasato Univ.School of Medicine Research Associate, 医学部, 助手 (70276054)
TAKEMURA Hisashi Kitasato Univ.School of Medicine Research Associate, 医学部, 助手 (70322435)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 2000: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1999: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | potassium channel / ROMK2 / ROMK1 / Kir7.1 / cardiac infarction / congenital heart failure / potassium load / rats / K^+チャネル / 心筋梗塞ラット / K^+負荷ラット / 腎髄質内層集合管 / NKCC1 mRNA / 高浸透圧 / ウエスタンブロット / cycloheximide |
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| Research Abstract |
It is known that abundance of the membrane transporter gene expression in kidney tubules changes during the period of either growing or aging. Its level is provably regulated by changes in the chemical or hormonal conditions of internal environment. Physiological and pathological changes in body fluid electrolytes, which are related with food intake, internal metabolism, and various diseases, may directly affect expression of the ion transporter mRNA.In order to investigate the factors which may regulate the gene expression, we have prepared two model animals : one is the potassium-loaded newborn rat and the other one is the rat with cardiac infarction. First, development of the renal potassium excretion capacity was studied in the newborn rats of 7-14 days which were acutely infused with the exogenous potassium. The onset of the extra potassium excretion was determined as 1.7 day. Time-course of the ROMK1 expression was in parallel increased with that of the extra potassium excretion. Time-courses of the ROMK2 and Kir7.1 expression were different. According to these results, a possible rate limiting step for potassium secretion is hypothesized as ROMK1 channel at the apical membrane of collecting ducts. Second, time-dependent changes in the expression of NHE1 mRNA and protein were investigated by using either RNase protection assay or Western blotting, respectively, in the rat with cardiac infarction. It seems to be strange that NHE1 protein decreased significantly at 5 h after the infarction, whereas NHE1 mRNA varied little in the same period. Decrease in sodium influx through a N+/H+ antiporter may protect the cardiac cell by decreasing ATP consumption of Na+/K+ ATPase. Regulation of the Na/K/2Cl transporter (NKCC2) mRNA expression by the secondary changes in electrolytes after cardiac infarction remains unsolved.
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