| Project/Area Number |
10670051
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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 | University of Occupational and Environmental Health |
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Principal Investigator |
HAYASHIDA Yoshiaki UOEH, Insti.Industri.Ecol.Sci., Professor, 産業生態科学研究所, 教授 (40047204)
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| Co-Investigator(Kenkyū-buntansha) |
MURASATO Yoshinobu UOEH, Insti.Industri.Ecol.Sci., Research Associate, 産業生態科学研究所, 助手 (40291843)
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| Project Period (FY) |
1998 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2000: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1999: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1998: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | nitric oxide / direct mesurement / hindquarter perfusion / SHR / endothelium-derived hyperpolarizing factor / acetylcholine / bradykinin / 後肢灌流系 / Aminoguanidine / 後肢潅流 |
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| Research Abstract |
1) We improved nitric oxide (NO) measuring system in the vascular perfusion of rat. NO was measured with NO direct-measuring systems (Model No.501, or Model MES-100) with each NO selective electrode. A calibration curve was prepared for each electrode in both Models using an NO standard solution. The electrodes detected more than 0.06 nmole of NO.
2) Acetylcholine (ACh) dose-dependently produced NO and concomitant vasodilation in the system. NO synthase inhibitor blocked NO release, but the vasodilation by ACh remained. The decrease in perfusion pressure (PP) in response to ACh was almost abolished in the presence of both L-NMMA and TEA or with deendothelialization. Bradykinin (BK) also induced NO release and biphasic effects on PP, which decreased with a lower concentration of BK and increased with a higher concentration. L-NMMA and TEA each abolished the decrease in PP induced by BK.In the presence of both L-NMMA and TEA, PP increased in response to BK.These results suggest that ACh and BK induce vasodilation through NO release and potassium channel dependent mechanism via endothelium.
3) NO release by vasoconstriction in response to norepinephrine (NE) was investigated using this system in a model of hypertension (SHR) and normal control (WKY) rats between 4 and 16-week age. We found a significant correlation between NO release and the increase in PP by vasoconstriction in WKY between 4 and 16-week age, but not in age-matched SHR.NOx excretion in WKY was greater at 4-week age than that in age-matched SHR, and gradually decreased with aging from 4 to 16-week age. Whereas, NOx excretion in SHR did not change from 4 to 12-week age, and then decreased at 16-week age to a level of that in age-matched WKY.These results show that NO release decreased with age in both WKY and SHR, and suggest that there might be abnormal endothelial function of NO production to vasoconstriction in SHR.
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