アンジオテンシンII型1受容体阻害はアルコール性心筋病を予防する
Che-Ping Cheng1, Heng-Jie Cheng, Carol Cunningham
1Cardiology Section, Department of Internal Medicine, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1045, USA. ccheng@wfubmc.edu
Circulation
|July 13, 2006
まとめ
アルコール摂取はレニン-アニオテンシン系 (RAS) を活性化させ,アルコール性心筋症を引き起こす. イルベサルタンでアンジオテンシンII (Ang II) 型1受容体 (AT1) をブロックすると,この心臓機能不全が予防されます.
科学分野:
- 心臓病学 心臓病学
- 薬理学 薬理学とは
- 毒理学 毒理学 毒理学
背景:
- アルコール性心筋症は,慢性的なアルコール摂取の潜在的な結果です.
- レニン-アニオテンシン系 (RAS) は,アルコール性心筋病の発達に役割を果たす可能性があります.
研究 の 目的:
- アルコール性心筋病の発生に対するアンジオテンシンII (Ang II) 型1受容体 (AT1) 阻害の影響を調査する.
- イルベサルタンがアルコールを飲ませた犬の心臓機能とRAS活性化に与える影響を評価する.
主な方法:
- 器具付きの犬は,アルコール,アルコールプラスイルベサタン,対照の3つのグループに分けられました.
- 左心室 (LV) と心筋細胞機能,およびRASマーカーを6ヶ月間モニタリングした.
- 測定には,LV収縮性,筋細胞短縮および再長縮,およびカルシウムトランジエントが含まれていました.
主要な成果:
- アルコール摂取は,持続的なRAS活性化につながり,Ang II,レニン活性,AT1受容体発現が増加したことが示されています.
- 心臓機能不全は,LV収縮性の低下,筋細胞機能の障害,カルシウム処理の低下として表れています.
- イルベサタン治療は,アルコールによる心臓機能不全を予防し,RAS活性化を抑制しました.
結論:
- 慢性的なアルコール摂取はRASを活性化し,進行的な心臓機能障害を引き起こします.
- AT1受容体阻害は,アルコール性心筋病の発生を効果的に防ぐことができます.
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