| Project/Area Number |
14571578
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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 |
Obstetrics and gynecology
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| Research Institution | Nagoya City University |
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Principal Investigator |
SUZUKI Yoshikatsu Nagoya City University, Graduate School of Medical Sciences, Associate Professor, 大学院・医学研究科, 助教授 (30254288)
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| Co-Investigator(Kenkyū-buntansha) |
SUZUMORI Kaoru Nagoya City University, Graduate School of Medical Sciences, Professor, 大学院・医学研究科, 教授 (80117829)
ITOH Takeo Nagoya City University, Graduate School of Medical Sciences, Professor, 大学院・医学研究科, 教授 (70159888)
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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 |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2003: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2002: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Preeclampsia / Endothelial function / Superoxide |
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| Research Abstract |
In our previous study, the reduced function of nitric oxide (NO) produced by endothelial cells was found in omental resistance arteries. The underlying mechanism was caused by not reduced production but down-regulation of cGMP, the 2nd messenger of NO (Suzuki et al.,2000).
In this study, we investigated the changes in other endothelium derived relaxing factors, such as prostacyclin and endothelium-derived hyperpolarizing factor (EDHF) in same artery. The reduced function of endothelial prostacyclin was obvious due to the reduction of producing prostacyclin in preeclampsia. By use of conventional microelectrode technique, the membrane potential was not changed in preeclampsia (Suzuki et al. 2002). These results suggested that in preeclampsia, the function not only of NO but also prostacyclin is down-regulated, while the function of EDHF remains normal. Furthermore, it was found that the morphological change in endothelial cell is not present in preeclampsia (Suzuki et al.,2003). We investigated the mechanism of down-regulation of cGMP by use of nitoriglycerin (NTG)-tolerant rabbit. It was found that the function of cGMP is reduced by superoxide (Nakano et al. 2004).
In the future, we will clarify with this reduction, focusing on the increase in superoxide via activation of angiotensin II type 1 receptor in resistance artery in both NTG-tolerant rabbit and preeclampsia.
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