Elucidation of cardiac muscle fibrosis mechanism by renin-angiotensin system through chymase
| Project/Area Number |
16580268
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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 |
Clinical veterinary science
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| Research Institution | Kitasato University |
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Principal Investigator |
UECHI Masami Kitasato University, Facaulty of Veterinary Medicine and Animal Sciences., 獣医畜産学部, 助教授 (90296426)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 2005: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2004: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | heart failure / hamster / cardiac fibrosis / renin-angiotensin system / angiotensin receptor / aldosteron / 心筋線維化 / レニン-アンジオテンシン |
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| Research Abstract |
In chronic heart failure, renin- angiotensin (RAS) system is enhanced. Angiotensin converting enzyme and chymase are present in RAS system, and these enzymes may affect pathophysiologically in cardiac failure. In this study, response to tissue RAS of ACE inhibitor (enalapril) and Ang II type receptor blocker (ARB : Candesartan) were examined. Hamsters with an aortic coarctation were given ACE inhibitor and ARB. Cardiac muscle hyperplasia depression was observed in ACE inhibitor and ARB administrated group by echocardiography, and the decrease that was significant in heart / body weight ratio was observed. The left ventricle ACE and the chymase activity were not inhibited by ACE inhibitor and ARB. However, decreased systolic blood pressure and decrease of left ventricle Ang II were observed by ACE inhibitor and ARB, and this tendency was more massive in a combined medication. These results suggested increasing afterload and tissue Ang II contribute cardiac hypertrophy in pressure overload.
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Report
(3 results)
Research Products
(14 results)
