| Project/Area Number |
09672347
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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 |
Laboratory medicine
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| Research Institution | HIROSAKI UNIVERSITY |
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Principal Investigator |
YASUJIMA Minoru Hirosaki University, School of Medicine, Professor, 医学部, 教授 (90142934)
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| Co-Investigator(Kenkyū-buntansha) |
SHOJI Masaru Department of Laboratory Medicine, Hirosaki University School of Medicine, Instructor, 医学部, 助手 (10226300)
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| Project Period (FY) |
1997 – 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: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | gene polymorphism / hypertension / restriction enzyme fragment length polymorphism (RFLP) / angiotensinogen / angiotensin converting enzyme / angiotensin II type 1 receptor / cardiovascular diseases / end-stage renal disease / 高血圧 / 脳卒中 / アンジオテンシノーゲン遺伝子多型 / アンジオテンシンII1型受容体遺伝子多型 / 糖尿病性腎症 / 糸球体腎炎 / 終末期腎不全 / 維持血液透析 / アンジオテンシン変換酵素遺伝子多型 / 糖尿病 / 高脂血症 |
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| Research Abstract |
The renin-angiotensin system (RAS) plays an important role in the regulation of blood pressure and regional blood flow. Gene polymorphisms of 3 major components of the RAS, angiotensinogen, angiotensin converting enzyme (ACE) , and angiotensin II type 1 receptor (AT1R) have been raised as possible genetic markers for hypertension and its complications. The mortality and morbidity of hypertension and hypertensive cardiovascular diseases are high in the Aomori population. Therefore, we tried to identify the prevalence of significant 3 gene variants of those components in hypertensive and normotensive subjects living in Aomori prefecture. Patients with end-stage renal disease (ESRD) and patients with cerebrovascular diseases were also enrolled in this study. Positive linkages were identlfied between hypertension and 2 gene polymorphisms including angiotensinogen M235T and ACE I/D. However, disequilibriums in AT1R A1166C polyrrmorphism was absent between hypertensive and normotensive groups. ACE I/D was also associated with cerebrovascular diseases, but not with ESRD.
These results suggest that the angiotensinogen M235T and ACE I/D variants may be genetic-susceptibility factors for hypertension and that ACE I/D may further contribute to cerebrovascular diseases as a genetic marker in the Aomori population.
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