| Project/Area Number |
10470008
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| Research Category |
Grant-in-Aid for Scientific Research (B).
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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 | Kagawa Medical University |
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Principal Investigator |
KOSAKA Hiroaki Kagawa Medical Univ. Physiology, Professor, 医学部, 教授 (60158897)
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| Co-Investigator(Kenkyū-buntansha) |
YONEYAMA Hirohito Kagawa Medical Univ. Physiology, Assistant Professor, 医学部, 助手 (80294750)
FUJII Shigemoto Kagawa Medical Univ. Physiology, Assistant Professor, 医学部, 助手 (00325333)
YAMAMOTO Akira Kagawa Medical Univ. Physiology, Assistant Professor, 医学部, 助手 (70314911)
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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 |
¥13,700,000 (Direct Cost: ¥13,700,000)
Fiscal Year 2000: ¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 1999: ¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 1998: ¥7,400,000 (Direct Cost: ¥7,400,000)
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| Keywords | NO / superoxide / mast cell / angitensin / migration / hypertension / EDCF / apoptosis |
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| Research Abstract |
Independently to mast cells, endogenous NO is physiologically operating to prevent vascular endothelium from oxidative stress and subsequent leukocyte adhesion and emigration, while mast cells play an essential role in the immune complex-mediated leukocyte adhesion and emigration. Thus next we examined the phenomenon to increase superoxide or to decrease NO.
Superfusion of angiotensin II (Ang II) ceased blood flow in rat mesenteric microcirculation, however, successive reflow occurred. Superoxide dismutase (SOD) significantly delayed the stoppage by Ang II and restored the successive reflow earlier. The acute reaction between Ang II and mesenteric artery induced immediate superoxide production when observed by a chemiluminescence method using Cypridina luciferin analog. The acute vascularsuperoxide production on addition of Ang II contributed to in vitro vascular contraction as it was significantly attenuated by SOD.The acute superoxide producing effect is likely to be specific to Ang II, because such significant modification by SOD was not observed for norepinephrine.
Impaired endothelium-dependent relaxation to acetylcholine is caused in part by induction of EDCF synthesis/release in renal arteries of hypertensivesalt-sensitive Dahl rats. L-Arginine, a substrate of nitric oxide synthase inhibitor, can attenuate sodium retention and development of hypertension, which lead to a decrease in EDCF synthesis in renal arteries.
We performed transient global ischemia in isolated rat hearts, followed by reperfusion. Cardiomyocytes showed apoptosis on reperfusion after warm ischemia, but not after cold ischemia. Caspase inhibitor can improve fractional shortening of the-left ventricle and to reduce cardiomyocyte apoptosis and the infarcted area induced by ischemia-reperfusion. We will examine effect of superoxide on the apoptosis.
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