| Project/Area Number |
06671661
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
NOZAKI Masahiro KYUSHU UNIV.FACULTY OF MED.LECTURER, 医学部, 助手 (60228319)
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| Co-Investigator(Kenkyū-buntansha) |
HASHIMOTO Kazunori KYUSHU UNIV.FACULTY OF MED.LECTURER, 医学部, 助手 (40264048)
INOUE Yoshihito KYUSHU UNIV.FACULTY OF MED.LECTURER, 医学部, 助手 (20260698)
SANO Masatoshi KYUSHU UNIV.FACULTY OF MED.SENIOR LECTURER, 医学部, 講師 (60206000)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1995: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1994: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | Estradiol / Vascular smooth muscle / Contraction / Relaxation / Ovarian steroids / 血管内皮 |
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| Research Abstract |
Effects of estradiol on the mechanical properties of the rabbit basilar artery and the rat mesenteric artery were investigated by use of isometric tension recording methods. Estradiol relaxd arterial tissue with intact endothelium pre-contracted by excess high-potassium solution in a concentrationdependent manner. In Ca-free solution, histamine and caffeine each produced a phasic contraction, but estradiol did not significantly affect their amplitude. Estradiol decreased the electrically induced contraction in a concentration dependent manner. Those contractions were inhibited in the presense of tetrodotoxin via perivascular nerve signal transduction system.
In the menopausal women, lipid metabolisms were worsened accoding to the duration of estrogen deficiency. On the other hand, lipid metabolisms were improved by hormone replacement therapy. These results suggest that estradiol relaxs arterial tissue via the endothelium dependent systems, and decreases the electrically induced contraction via perivascular nerve signal transduction systems. Moreover, estrogen supress the atherosclerotic change by improving lipid metabolisms.
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