| Project/Area Number |
13670762
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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 |
Circulatory organs internal medicine
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| Research Institution | Kansai Medical University |
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Principal Investigator |
MASAKI Hiroya Kansai Medical University, Department of Medicine, 准教授 (60298883)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUBARA Hiroaki Kyoto prefectural University of Medicine, Faculty of Medicine, 教授 (10239072)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2001: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | angiotensin II / angiotensin II Type 2 receptor / vascular smooth muscle / L-type Ca channel / left ventricular hypertrophy / cardiac fibrosis / 受容体 / イオンチャネル / イオンチャンネル |
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| Research Abstract |
【Purpose】 We reported that angiotensin II decreased blood pressure through a action of angiotensin II type II receptor in angiotensin II type II overexpression transgenic mouse. In this project, we are going to investigate the function of angiotensin II type II receptor on vascular smooth muscle cell ion channels.
【Method】 We isolated vascular smooth muscle cell from abdominal aorta of angiotensin II type II receptor overexpression transgenic mouse. We measured function of vascular smooth muscle cell ion channels by electrophysiological methods.
We also investigate the effect of angiotensin II type II receptor of heart in hemodialysis patients by administration of angiotensin I type II receptor antagonist.
【results】 Angiotensin II did not affect the function of vascular smooth muscle ion channels including L-type Ca channel and K channel in angiotensin II type II overexpression transgenic mouse compared to wild type mouse.
Angiotensin II type I receptor antagonist increased cardiac hypertrophy and cardiac fibrosis in 6 months compared to Ca channel blocker in hemodialysis patients. This effect did not dependent on blood pressure lowering effect, and also suggested the possibility that angiotensin II type II receptor increased cardiac hypertrophy and cardiac fibrosis.
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