通过氧化激活线粒体ATP依赖的通道,由氧化激活
1Institute of Molecular Cardiobiology, Johns Hopkins University, Baltimore, MD 21205, USA.
Circulation
|February 2, 2000
概括
氧化 (NO) 直接激活线粒体的依赖ATP的K ((+) (mitoK ((ATP)) 通道. 这一发现揭示了NO诱导心脏保护的新机制,并增强了二氧化的作用.
科学领域:
- 心血管生理学心血管生理学
- 线粒体生物学 线粒体生物学
- 细胞信号传递 细胞信号传递
背景情况:
- 氧化 (NO) 是一种可疑的缺血预调的媒介.
- 线粒体ATP依赖的K(+) (mitoK(ATP)) 通道是这个过程中的拟议效应器.
- 和mitoK (ATP) 通道之间的确切关系尚不清楚.
研究的目的:
- 研究一氧化 (NO) 对线粒体ATP依赖的K ((+) (mitoK ((ATP)) 通道的直接作用.
- 阐明NO信号与mitoK (ATP) 通道活动之间的机械联系.
主要方法:
- 线粒体的氧化还原潜力被测量在子心室肌细胞中,作为线粒体K(ATP) 通道开放的指标.
- 使用NO的S-nitroso-N-acetyl-DL-penicillamine (SNAP) 供体来评估NO的影响.
- 选择性mitoK(ATP) 通道阻断剂和NO吸尘器被用于确认特异性.
主要成果:
- 剂量依赖的SNAP氧化了线粒体矩阵,表明了mitoK(ATP) 通道的激活.
- 通过一种特定的mitoK ((ATP)) 通道阻断剂和一个NO吸尘器来阻断SNAP的作用.
- SNAP增强了二氧化的氧化作用,这是另一种mitoK(ATP) 通道开启剂.
结论:
- 氧化 (NO) 直接激活线粒体的依赖ATP的K ((+) (mitoK ((ATP)) 通道.
- NO增强了二氧化的通道开通能力.
- 这些发现确定了NO介导心脏保护和mitoK (ATP) 通道之间的新型机制联系.
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