| Project/Area Number |
09671006
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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 |
Psychiatric science
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| Research Institution | Keio University |
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Principal Investigator |
SHINTANI Futoshi Medicine, Neuropsychiatry, Assistant Professor, 医学部, 助手 (90276379)
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| Co-Investigator(Kenkyū-buntansha) |
NAKAKI Toshio Medicine, Pharmacology, Professor, 医学部, 教授 (30164148)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 2000)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1998: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1997: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | 6-nitronorepinephrine / Norepinephrine / Nitric Oxide / COMT / Anti 6-nitronorepinephrine antibody / ラット |
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| Research Abstract |
Vasoactivities of 6-nitronorepinephrine were investigated using rat aorta. 6-Nitronorepinephrine (> 100 microM) caused dose-dependent contraction in both endothelium-intact and -denuded aorta, although the latter showed greater contraction than the former. Prazosin (> 3 nM), an alphal-adrenoceptor antagonist, attenuated significantly the 6-nitronorepinephrine-induced contractions, there by suggesting the alphal-adrenoceptor involvement. Aortic rings prepared from reserpine-pretreated rats showed the 6-nitronorepinephrine-induced a contraction to the extent similar to those from untreated rats, suggesting that endogenous norepinephrine does not play a role in the 6-nitronorepinephrine-induced contraction. 6-Nitronorepinephrine (> 10 microM) potentiated norepinephrine-induced contraction only in the presence of endothelium. The augmentation was attenuated by catalase (1200 U/ml). H2O2 (10-300 microM) augmented the norepinephrine-induced contraction only in the endothelium-intact rat aortic rings. 6-Nitronorepinephrine attenuated significantly acetylcholine-induced relaxation. Catalase prevented the 6-nitronorepinephrine-induced inhibition of the acetylcholine-induced relaxation. These results suggest that 6-nitronorepinephrine has a weak alphal-adrenoceptor agonistic property and that the endothelium-dependent potentiation by 6-nitronorepinephrine of the norepinephrine-induced contraction is mediated through production of H2O2.
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