权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Research on a novel endogenous catecholamine, 6-nitronorepinephrine

新型内源性儿茶酚胺6-硝基去甲肾上腺素的研究

基本信息

批准号：
09680771
负责人：
NAKAKI Toshio
金额：
$ 2.3万
依托单位：
Teikyo University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
1997
资助国家：
日本
起止时间：
1997 至 1998
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09680771/
关键词：
nitric oxide catecholamine blood vessels catalase hydrogen peroxide カタラーゼスーパーオキシド NO

项目摘要

Vasoactivities of 6-nitronorepineplirine were investigated using rat aorta. 6-Nitronorepinephrine (>100 muM) caused dose-dependent contraction in both endothelium-intact and -denuded aorta, although the latter showed greater contraction than the former. Prazosin (>3 nM), an alpha_1-adrenoceptor antagonist, attenuated significantly the 6- nitronorepinephrine-induced contractions, thereby suggesting the alpha_1-adrenoceptor involvement. Aortic rings prepared from reserpine-pretreated rats showed the 6-nitronorepinephrine-induced a contraction tothe 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 muM) potentiated norepinephrine-induced contraction only in the presence of endothelium. The augmentation was attenuated by catalase (1,200U/ml). H_2O_2 (10-300 muM) augmented the norepinephrine-induced contraction only in the endothelium-intact rat aortic rings. 6-Nitronorepinephrine attenuated significantly acetyicholine-induced relaxation. Catalase prevented the 6-nitronorepinephrine-induced inhibition of the acetylcholine-induced relaxation. These results suggest that 6-nitronorepinephrine has a weak txi-adrenoceptor agonistic property and that the endothelium-dependent potentiation by 6-nitronorepinephrine of the norepinephrine-induced contraction is mediated through production of H_20_2. Roles of superoxide in the formation of 6-nitronorepinephrine and distribution of the amine in the brain are being currently investigated.

用大鼠主动脉观察6-硝基肾上腺素的血管活性。6-硝基肾上腺素（bbb100 muM）在内皮完整和剥脱主动脉中均引起剂量依赖性收缩，尽管后者比前者收缩更大。α _1-肾上腺素受体拮抗剂Prazosin （bbb3nm）可显著减弱6-硝基肾上腺素诱导的收缩，从而提示α _1-肾上腺素受体参与其中。利血平预处理大鼠主动脉环显示6-硝基肾上腺素诱导的收缩程度与未处理大鼠相似，提示内源性去甲肾上腺素在6-硝基肾上腺素诱导的收缩中不起作用。6-硝基肾上腺素（bbb10mum）仅在内皮存在的情况下增强去甲肾上腺素诱导的收缩。过氧化氢酶（1200u /ml）对扩增有减弱作用。H_2O_2 （10-300 muM）仅在内皮完整的大鼠主动脉环中增强去甲肾上腺素诱导的收缩。6-硝基肾上腺素显著减弱乙酰胆碱引起的松弛。过氧化氢酶阻止6-硝基肾上腺素诱导的对乙酰胆碱诱导的松弛的抑制。上述结果表明，6-硝基肾上腺素对去甲肾上腺素有微弱的拮抗作用，6-硝基肾上腺素对去甲肾上腺素诱导的收缩的内皮依赖性增强作用是通过产生H_20_2介导的。目前正在研究超氧化物在6-硝基肾上腺素的形成和胺在大脑中的分布中的作用。