内源性血管过氧化调节动脉张力 in vivo
Tatsiana Suvorava1, Nadine Lauer, Stephanie Kumpf
1Institut für Pharmakologie und Klinische Pharmakologie, Heinrich-Heine-Universität, 40225 Düsseldorf, Germany. kojda@uni-duesseldorf.de
Circulation
|October 12, 2005
概括
内源性过氧化 (H2O2) 可能会缩小血管. 在血管组织中H2O2减少的小鼠表现出较低的血压,这表明H2O2在体内调节血压.
科学领域:
- 心血管生理学心血管生理学
- 氧化压力生物学 氧化压力生物学
背景情况:
- 实验室研究表明,过氧化 (H2O2) 有直接的血管运动作用.
- 在体内,H2O2的血管运动效应在很大程度上是未知的.
研究的目的:
- 研究内源性过氧化 (H2O2) 在血管度和血压调节中的体内作用.
- 为了确定H2O2是否在阻力血管中起到血管收缩作用.
主要方法:
- 在血管组织中产生过度表达catalase的转基因小鼠 (cat++).
- 评估了催化酶mRNA,蛋白质和血管组织中的活性.
- 大动脉内皮和心肌中的量化反应性氧物种.
- 在猫++和对照小鼠中测量了缩血压 (sBP).
- 服用催化酶和氧化合成酶抑制剂,以评估H2O2的作用.
主要成果:
- 血管催化酶过度表达显著减少了活性氧物种.
- 与对照组相比,Cat++小鼠的系统血压显著降低.
- 酶抑制增加了猫++小鼠的sBP,使其正常化到控制水平.
- 氧化合成酶抑制在两组中同样影响了sBP.
- 在猫++小鼠中,内皮和NO依赖的血管扩张保持不变.
- 在猫++小鼠中,大动脉收缩到KCl和外源H2O2的减少.
结论:
- 内生H2O2可能在抵抗血管中起到血管收缩作用.
- H2O2有助于在体内调节血压.
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