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急性および慢性アンジオテンシン-1受容体アンタゴニズムは,動脈硬化症における内皮機能不全を逆転させます
A Prasad1, T Tupas-Habib, W H Schenke
1Cardiology Branch, Office of Biostatistics Research, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Circulation
|May 24, 2000
まとめ
ロサルタンによるアンジオテンシン-1 (AT(1)) 受容体阻害は,窒素酸化物の可用性を高めることで,動脈硬化症患者の内皮機能不全を改善した. これは,AT(1) 受容器の阻害が動脈硬化症の治療上の利点を提供することを示唆しています.
科学分野:
- 心血管医学 心血管医学
- 薬理学 薬理学とは
- 血管生物学 血管生物学
背景:
- レニン-アニオテンシン系は,内皮機能不全を促進することによって,アテロゲネシスに役割を果たします.
- アンジオテンシン-1 (AT(1)) 受容体阻害は,内皮機能を改善する可能性について調査されています.
研究 の 目的:
- 動脈硬化症の患者の内皮機能不全を改善するかどうかを決定する.
- ロサルタンがマイクロ血管応答と血管拡張に与える影響を評価する.
主な方法:
- 血管活性剤に対する微血管反応は,動脈硬化症の患者および動脈内ローサルタン投与前のおよび後の対照群で研究されました.
- 流動介的腕動脈の血管拡張は,口服ロサルタン治療の8週間後に超音波を用いて評価されました.
- 血清中の酸化窒素濃度が測定されました.
主要な成果:
- 静脈内ローサルタンは,アンジオテンシンII媒介の血管収縮を阻害し,アセチルコリン誘発の血管拡張を増加させた患者で投与された.
- 経口ロサルタン療法は,フローメディエートされた腕動脈の拡張を改善し,血清酸化窒素濃度を増加させた.
- 反応性高血症に対する反応は強化され,ナトリウムニトロプルスシドとニトログリセリンの反応は変化しなかった.
結論:
- AT(1) 受容体の阻害は,動脈硬化症患者の内皮機能不全を逆転させます.
- 改善された酸化窒素の利用可能性は,観察された利点の重要なメカニズムです.
- AT(1) 受容体阻害は,動脈硬化症の長期的な治療的可能性を秘めている可能性があります.
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