| Project/Area Number |
11670697
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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 | Yokohama City University |
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Principal Investigator |
UEDA Shinichiro Yokohama City University School of Medicine, Research Associate., 医学部, 助手 (80285105)
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| Co-Investigator(Kenkyū-buntansha) |
GOTO Eiji Yokohama City University School of Medicine, Assistant Prof, 医学部, 助教授 (30153753)
TOYA Yoshiyuki Yokohama City University School of Medicine, Assistant Prof, 医学部, 講師 (30237143)
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| Project Period (FY) |
1999 – 2000
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 2000: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1999: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | angiotensin (1-7) / angiotensin II / angiotensin I / ACE / nitric oxide / ACE inhibitor / ブラジキニン / アンジオテンシンII / アンジオテンシン変換酵素 / 本態性高血圧 / アンジオテンシン(1-7) / 一酸化窒素 / 前腕抵抗血管 |
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| Research Abstract |
We investigated effects of angiotensin peptide in human forearm resistant vessles in vivo. We also established the assay system of angiotensin peptides and evaluated effects of angiotensin converting enzyme (ACE) inhibitor on plasma concentration of angiotensin (1-7) in normotensive and hypertensive subjects.
1. Angiotensin (1-7) had no direct vasodilating effect in human forearm resistant. However, angiotensin (1-7) antagonized angiotensin II but not noradrenaline induced vasoconstriction, which suggested that angiotensin (1-7) might act as an endogenous angiotensin II antagonist.
2. Angiotensin (1-7) significantly potentiated bradykinin-induced vasodilatation in human forearm resistant vessels. This effect was abolised by L-NMMA, nitric oxide synthase inhibitor, which suggested the involvement of nitric oxide in this interaction
3. Angiotensin (1-7) induced potentiation of the vasodilating effect of bradykinin was also abolished by the single dose of ACE inhibitor., which suggested ACE dependent effect of angiotensin (1-7) on bradykinin. Angiotensin (1-7) also significantly attenuated angiotensin I-induced vasoconstriction. These results suggested that angiotensin (1-7) might be an endogenous ACE inhibitor in man.
4. Chronic treatment with ACE inhibitors was associated with significant increased levels of plasma angiotensin (1-7) levels but not decreased levels of plasma angiotensin II in patients with essenstila hypertension. Angiotensin (1-7) may contribute to maintenance of hypotensive effect of ACE inhibitors in man.
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