| Project/Area Number |
25460877
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Legal medicine
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| Research Institution | Nara Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
KUDO Risa 奈良県立医科大学, 医学部, 助教 (20347545)
MORIMURA Yoshifumi 奈良県立医科大学, 医学部, 助教 (50305710)
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| Project Period (FY) |
2013-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2015: ¥520,000 (Direct Cost: ¥400,000、Indirect Cost: ¥120,000)
Fiscal Year 2014: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2013: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | アルコール / ラット / 上腸間膜動脈 / 一酸化窒素 / 内皮由来過分極因子 / 等尺性張力 / 当尺性張力 |
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| Outline of Final Research Achievements |
The endothelium-dependent relaxation (EDR) in response to acetylcholine (Ach) was greater in ethanol-fed rats than that in the controls. In the combined presence of endothelium-derived hyperpolarizing factor (EDHF) inhibitors, the relaxation response to Ach did not differ significantly between the two groups. Furthermore, neither A23187, which causes EDR in a manner unrelated to any receptor mechanism, nor levcromakalim, which activates the KATP channel on smooth muscle membranes, caused an increased EDR in ethanol-fed rats. These results suggest that the increased EDR in response to Ach in ethanol-fed rats may be caused by the increase in EDHF-mediated relaxation response. Thus, the present study suggests that the endothelium can exert a protective effect during chronic ethanol-induced hypertension through the EDHF-mediated backup system.
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