| Project/Area Number |
13670688
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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 | Gunma University |
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Principal Investigator |
SAKAMAKI Tetsuo Gunma University School of Medicine, Professor, 医学部, 教授 (20124654)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAMURA Tetsuya Gunma University School of Medicine, Associated professor, 医学部, 助教授 (10272238)
KANDA Tsugiyasu Kanazawa Medical University, Professor, 医学部, 教授 (40261838)
MIZUNUMA Hideki Hirosaki University School of Medicine, Professor, 医学部, 教授 (10125875)
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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 |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2002: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2001: ¥2,600,000 (Direct Cost: ¥2,600,000)
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| Keywords | estrogen / menopause / women / hypertension / hypertrophy / bradykinin / polyunsaturated fatty acid / ambulatory blood pressure / 閉経後女性 / アンジオテンシン変換酵素 / 血清脂質 / ホルモン / 退縮 |
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| Research Abstract |
In order to clarify the mechanisms by which hormone replacement therapy (HRT) prevents cardiovascular disease (CVD), we investigated 1) the effects of 12-month HRT [conjugated equine estrogen 0.625 mg + medroxyprogesterone acetate 2.5 mg daily] on left ventricular hypertrophy (LVH) and growth-promoting factors in hypertensive postmenopausal women (PMW) with LVH, 2) whether the angiotensin-converting enzyme (ACE) genotype affects the HRT-induced decrease in serum ACE activity in PMW and whether the increase in plasma bradykinin is dependent on the ACE-genotype, 3) the effects of HRT on plasma docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) in PMW, and 4) the effects of HRT on office blood pressure (BP) and 24-hour ambulatory blood pressure (ABP) in hypertensive PMW. In results, 1) HRT reduces LVH in hypertensive PMW without association with the changes in growth-promoting factors. 2) HRT reduced ACE activity in ACE I/D and D/D groups, but not in I/I group. HRT increased bradykinin in all groups. 3) HRT increased DHA and EPA in PMW. 4) HRT did not alter office BP, ABP or the proportion of nondippers in hypertensive PMW. In conclusion, 1) Without being associated with changes in systemic growth-promoting factors, HRT-induced regression of LVH in hypertensive PMW may be partly beneficial effects of HRT on CVD. 2) Decrease in ACE activity and increase in bradykinin by HRT may represent beneficial effects of HRT on CVD. 3) Increases in DHA and EPA by HRT could be associated with the antiatherosclerotic effects of HRT in PMW. 4) With respect to BP, HRT might not be harmful in hypertensive PMW whose BP has been well-controlled before HRT.
In the present study, we represented the several possible mechanisms by which HRT prevents CVD.
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