心臓アンジオテンシン-(1-7) が発作性心筋病症の治療に用いられる
David B Averill1, Yuichiro Ishiyama, Mark C Chappell
1The Hypertension and Vascular Disease Center, Wake Forest University School of Medicine, Medical Center Blvd, Winston-Salem, NC 27157, USA. daverill@wfubmc.edu
Circulation
|October 1, 2003
まとめ
心筋梗塞の後に,ペプチドアンジオテンシン-1-7 (Ang-[1-7]) の発現はネズミの心臓ミオサイトで増加する. この発見は,Ang-(1-7) が心不全に対する心臓の反応に役割を果たしていることを示唆しています.
科学分野:
- 心血管生理学 心血管の生理学
- 腎臓系と高血圧について
- 分子心臓病学 分子心臓病学
背景:
- アンジオテンシン1-7) (Ang-[1-7]) は,心臓におけるアンジオテンシンIIの効果を抑える.
- 心筋梗塞 (MI) モデルにおけるAng-(1-7) 発現の調査は極めて重要です.
研究 の 目的:
- ネズミの心筋梗塞後の心筋梗塞におけるAng-(1-7) 発現を決定する.
- Ang-(1-7) の心臓組織における細胞の局所性を理解する.
主な方法:
- ルイス・ラットの冠動脈連動によって誘発された心筋梗塞.
- ヘモダイナミックパラメータと心筋縮は,MIの4週間後に評価された.
- Ang-(1-7) に対する免疫反応は,心筋細胞,インタースティシャル細胞,血管に局限する.
主要な成果:
- MIのマウスは,左心室の末端ダイアストリック圧力が上昇し,シストリック圧力が低下した.
- MIを患ったマウスの心臓に顕著な心筋縮が観察されました.
- Ang-(1-7) 免疫反応は,心臓発作領域を取り巻く心室組織で有意に増加した.
結論:
- 冠動脈連動後の心不全はAng-(1-7) 発現を増加させる.
- 増加したAng-(1-7) は,心筋細胞内でのみ局在する.
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