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Gad A Silberman1, Tai-Hwang M Fan, Hong Liu

  • 1Department of Medicine (Division of Cardiology), Emory University School of Medicine, Atlanta, GA, USA.

Circulation
|January 20, 2010
PubMed
まとめ

テトラヒドロビオプテリン (BH(4)) の欠乏は,高血圧における心臓の酸化と静脈動脈機能不全に寄与する. BHを補充すると,心臓機能が改善され,発射分子が保存された心不全の潜在的な治療法として示唆されます.

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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
  • 薬理学 薬理学とは

背景:

  • 高血圧は心不全の主要な原因であり,心筋放出分子が保たれ,心筋のダイアストリックリラクゼーションが損なわれることが特徴です.
  • 配合されていないNO合成酵素 (NOS) による窒素酸化物 (NO) の生物利用性の低下は,しばしばテトラヒドロビオプテリン (BH(4) の枯渇によって引き起こされ,ダイアストリック機能不全に関連しています.
  • 酸化ストレスとBH(4) 欠乏症は,血管系効果とは無関係に心臓のダイアストリック機能を損なう可能性があります.

研究 の 目的:

  • 心臓の酸化とBHの欠乏が,高血圧に起因する腹動力機能不全における役割を調査する.
  • 縮機能不全に対するBH(4) 補給の治療の可能性を調査する.

主な方法:

  • 高血圧マウスモデル (片側腎切除,デオキシコルチコステロンアセテートペレット,塩分飲料) を用いて,心臓機能,酸化,NOS結合を評価した.
  • 測定された心臓のBH(4) レベル,酸化バイオプテリン,NOと超酸化物産生,およびフォスフォランバン・フォスフォリレーション.
  • 高血圧マウスにBH(4) を投与し,心臓機能と分子マーカーに対する効果を評価した.
  • リラクゼーション特性を評価するために,孤立した心筋細胞実験を行った.

主要な成果:

  • 高血圧のマウスは,下痢性機能障害,心臓酸化,心臓のBHの減少,およびNOの生産が減少した結合されていないNOSを示した.
  • BH(4) 補給は受けましたが,ヒドララジンやテトラヒドロネオプテリンは受けていませんが,心臓のBH(4) レベルが改善され,フォスフォランバンのリン酸化とダイアストリック機能が改善されました.
  • 単離された心筋細胞は,BH治療によって正常化された緩和障害を示した.
  • 心臓特異的なアニオテンシン変換酵素の過剰発現は,似たような酸化性および下痢性機能不全のフェノタイプを誘発した.

結論:

  • 血管系因子とは無関係な心臓の酸化は,不結合のNOSとダイアストリック機能不全を引き起こす可能性があります.
  • テトラヒドロビオプテリン (BH(4)) 補充は,高血圧に関連した静脈機能不全に対する有望な治療戦略です.