| Project/Area Number |
05454267
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Shiga University of Medical Science |
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Principal Investigator |
IWAI Naoharu Shiga Univ.of Med Sci.First Dept of Int Med., Assistant, 医学部, 助手 (30242978)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥6,800,000 (Direct Cost: ¥6,800,000)
Fiscal Year 1994: ¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1993: ¥4,500,000 (Direct Cost: ¥4,500,000)
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| Keywords | SA gene / Angiotensinogen gene / Angiotensin I converting enzyme gene / hypertension / genetics / ventricular hypertrophy / ventricular remodeling / genetics / hypertension / 遺伝 / アンジオテンシノーゲン |
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| Research Abstract |
We assessed whether SA gene locus might be also involved in pathogenesis of hypertension in human essential hypertension, and also assessed whether gene polymorphism in angiotensin converting enzyme and angiotensinogen might be involved in pathogenesis of several cardiovascular diseases.
1. We determined the sequence of human SA cDNA and confirmed that this gene was located on human chromosome 16p13-11. Association study between this gene locus and hypertension was performed employing Pst I restrication fragment length polymorphism. In our Japanese hospital-based population, the frequency of the minor allele of this gene was significantly higher in hypertensive subjects than in that in normotensive subjects. According to our collegues in Australia, the frequency of the minor allele seems to be higher in obesitic hypertensive subjects than that in obestic normotensive subjects, which is being pursued by them.
2. TT genotype of the angiotensinogen gene was a risk factor of juvenile-onset hypertension in our Japanese population, and high body mass index was risk factor of late-onset hypertension.
3. WE have confirmed that DD geneotype of the angiotensin converteing enzyme gene is a risk factor of left ventricular hypertrophy and a risk factor of subsequent left ventricular dysfunction after myocardial infarction.
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