血管内産の過酸化水素は,動脈の緊張をin vivoで調節する
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
まとめ
固有の過酸化水素 (H2O2) は血管を収縮させる可能性があります. 血管組織にH2O2が減少したマウスは血圧が低下し,H2O2が血液圧をin vivoで調節することを示唆しました.
科学分野:
- 心血管生理学 心血管生理学
- 酸化ストレス生物学 生物学
背景:
- 実験室内研究では,過酸化水素 (H2O2) が血管運動に直接的な効果があることが示唆されています.
- H2O2の in vivo 血管運動効果は,ほとんど不明のままである.
研究 の 目的:
- 血管トーンと血圧の調節における内生性過酸化水素 (H2O2) のインビヴォの役割を調査する.
- H2O2が抵抗容器の血管圧縮剤として作用するかどうかを判断する.
主な方法:
- 血管組織 (cat++) でカタラゼを過剰発現するトランスジェニックマウスを生成した.
- 評価されたカタラゼ mRNA,タンパク質,および血管組織における活性.
- 大動脈内皮と心筋内皮における量化反応性酸素種.
- 猫++と対照マウスのシストリック血圧 (sBP) の測定.
- H2O2の役割を評価するために,カタラーゼおよび酸化窒素合成酵素阻害剤を投与した.
主要な成果:
- 血管カタラーゼ過剰発現により,活性酸素種が著しく減少した.
- Cat++マウスは,対照群と比較して,シストリック血圧が著しく低下した.
- カタラーゼ阻害は,猫++マウスのsBPを増加させ,コントロールレベルに正常化させました.
- 酸化窒素合成酵素の阻害は,両方のグループで同様にsBPに影響を与えました.
- 内皮およびNO依存性血管拡張は,猫++マウスでは変化しませんでした.
- 動脈の収縮がKClと外因的なH2O2に減少したのは,猫++マウスでした.
結論:
- 内生的なH2O2は,抵抗器の血管収縮剤として機能する可能性が高い.
- H2O2は,体内の血圧の調節に寄与する.
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