| Project/Area Number |
14572049
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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 |
Biological pharmacy
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| Research Institution | Tohoku University |
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Principal Investigator |
YOSHIDA Makoto Tohoku University, Graduate School of Pharmaceutical Sciences, Associate Professor, 大学院・薬学研究科, 助教授 (90201011)
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| Co-Investigator(Kenkyū-buntansha) |
OHKUBO Satoko Tohoku University, Graduate School of Pharmaceutical Sciences, Research Instructor, 大学院・薬学研究科, 助手 (20274954)
NAKAHATA Norimichi Tohoku University, Graduate School of Pharmaceutical Sciences, Professor, 大学院・薬学研究科, 教授 (60045804)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2003: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 2002: ¥2,800,000 (Direct Cost: ¥2,800,000)
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| Keywords | Hypertension / Pressure-natriuresis] / Adngiotension / 庄-利尿 |
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| Research Abstract |
Pressure-natriuresis relationship curve was determined from systolic blood pressure and urine secretion rate of rats fed normal or high-sodium containing diets for one week in individual metabolic cages. In comparison to normal Wistar rats, the pressure-natriuresis curves were shifted to the right in spontaneously hypertensive rats, Dahl salt-sensitive rats and DOCA-salt hypertensive rats. In addition to the rightward shift, the decrease in the elevation of the pressure-natriuresis curves in Dahi salt-sensitive rats and DOCA-salt hypertensive rats suggest that the salt-dependency of these hypertensive models. Oral administration of angiotensin converting enzyme inhibitor to spontaneously hypertensive rats decreased the elevation of the pressure-natriuresis curve but angiotensin type 1 receptor blocker or calcium antagonist shifted the curve to the left without changing the elevation. The administration of angiotensin converting enzyme inhibitor shifted the pressure-natriuresis curve to
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the left in Dahl salt-sensitive rats and did not affect the curve in DOCA-salt hypertensive rats. Acute administration of angiotensin type II receptor blocker increased the urine flow rate in anesthetized spontaneously hypertensive rats that was fed high-sodium containing diets for one week and also administered angiotensin type I receptor blocker for this period. To clarify the role angiotensin type II receptor in the pressure-natriuresis curves, we further examined the functions of this receptor in the primary cell culture of rat renal tubules. The mRNA level of angiotensin type II receptor was one to tenth of that of angiotensin type I receptor in adult rats and higher in five-days-old rats. The stimulation of angiotensin type II receptor in the primary culture from kidney of five-days-old rats induced the phosphorylation of extracellular signal-regulated kinase. Further investigation of the relationship between this phosphorylation and the pressure-natriuresis curves will be required for future. Less
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