| Project/Area Number |
10671742
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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 |
Functional basic dentistry
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| Research Institution | KYUSHU UNIVERSITY |
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Principal Investigator |
HORINOUCHI Yasufumi Kyushu Univ, Dentistry, Research Associate, 歯学部, 助手 (80219229)
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| Co-Investigator(Kenkyū-buntansha) |
SHIRASUNA Kanemitsu Kyushu Univ, Dentistry, Professor, 歯学部, 教授 (30093420)
KUBOTA Yasutaka Kyushu Univ, Dentistry, Research Associate, 歯学部, 助手 (60205151)
ISHIBASHI Hiroaki Kyushu Univ, Dentistry, Research Associate, 歯学部, 助手 (90254630)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1998: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | endothelial cell / Angiotensin II / VEGF / Ca-activated Cl channel / NO / カルシウム / 血管新生 / 血管内皮細胞増殖因子 |
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| Research Abstract |
The effect of Angiotensin II and VEGF on endothelial cells was investigated by using rat pulmonary artery. In the contraction measurement, VEGF had no effect on tissues. However, Angiotensin II significantly induced contraction in the rat pulmonary artery. The tissue with endothelial cells contracted phasically. On the other hand, phasic and tonic contraction was observed in the tissue without endothelial cell. Furthermore, in the presence of L-nitro-arginin, Angintensin II induced phasic and tonic contraction even in the tissue with endothelial cells. These results indicate the possibility of NO synthesis of the endothelial cells by Angiotensin II.
Next, the effect of VEGF and Angiotensin II on ion channels of the endothelial cells were investigated. VEGF had no effect on ion channel of the endothelial cell, on the other hand Angiotensin II induced phasic inward current in the whole cell configuration. This inward current was blockod by niflumic acid and was not observed in the presence of heparin in the electrode. Therefore, this inward current was suggested to be induced by the activation of Ca-activated Cl channel. This current was inhibited by the additional application of Angiotensin II inhibitor, TCV116. Taken together, Angiotensin II binds with AT1 receptor and Ca is released from SR via IP3 formation.
The prolifiration of the endothelial cell were significantly increased in the presence of 100nM Angiotensin II. This increase was completely inhibited by the additional application of TCV116. More interestingly, the prolifiration was inhibited only by the application of TCV116 compared with the control. This result suggested that Angiotensin II had autocline or paracline system in the endothelial cell.
In conclusion, Angiotensin II is suggested to have multiple function in the endothelial cells of rat pulmonary artery.
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