炎症促進媒介体は,窒素酸化物/循環性GMPに依存するメカニズムを通じて,動脈内の内皮由来ハイパーポラライジングファクターの形成を慢性的に下調調調節する
1Institut für Kardiovaskuläre Physiologie und Institut für Anaesthesiologie, Klinikum der J.W.G.-Universität, Frankfurt/Main, Germany.
Circulation
|April 13, 1999
まとめ
炎症促進媒介剤は,酸化窒素合成酵素II (NOS II) を誘導することによって,動脈におけるエンドセリウム由来高極化因子 (EDHF) の形成を阻害する. このEDHFの減少は,動脈硬化症や敗血症などの疾患における内皮機能不全に寄与する.
科学分野:
- 血管生物学 血管生物学
- 内皮機能の機能について
- 炎症 炎症 炎症 炎症 炎症
背景:
- 内皮に依存する膨張反応には,酸化窒素 (NO) とEDHFが含まれます.
- これらの反応は,動脈硬化症と敗血症で変化します.
- 炎症促進媒介体は,誘導可能なNO合成酵素 (NOS II) を通してEDHF生成に影響を与える可能性があります.
研究 の 目的:
- 孤立した動脈におけるEDHF発生に対するプロ炎症媒体の効果を調査する.
- NOS II表現がEDHF形成に影響するかどうかを判断する.
主な方法:
- 隔離されたウサギの頸動脈と豚の冠動脈は,サイトカインとリポポリサッカリドにさらされた.
- 酸化窒素合成酵素 (NOS) とサイクロオキシゲネーゼが阻害されました.
- NOS II表現とEDHF媒介のリラックスが評価されました.
- 血管の滑らかな筋肉細胞のハイパーポラライゼーションが測定されました.
主要な成果:
- 炎症促進媒介剤はEDHF媒介によるリラックスを著しく弱め,NOS II発現と一致しました.
- NOS IIまたはタンパク質合成の阻害は,この鈍化した緩和を防ぐことができました.
- NOのドナーは,炎症促進媒介体の効果を模倣した.
- 炎症促進媒介剤は,EDHFの合成を低下させ,シトクロームP450酵素の発現を低下させた.
結論:
- 炎症促進媒介剤は,孤立した動脈でEDHFの形成を阻害する.
- この阻害はNOS II発現と関連しており,誘導されたNO生成によって媒介される可能性が高い.
- EDHF形成の減少は,動脈硬化症と症における内皮機能不全に寄与する可能性があります.
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