アンジオテンシン変換酵素の活性に対する組織抑制は,血管新生を活体内で刺激する
J E Fabre1, A Rivard, M Magner
1Departments of Medicine (Vascular Medicine) and Biomedical Research, St Elizabeth's Medical Center, Tufts University School of Medicine, Boston, MA, USA.
Circulation
|June 15, 1999
まとめ
クイナプリラトによるアニオテンシン変換酵素 (ACE) 阻害は,後肢不全症のウサギの血管新生を強める. これは,高い組織親和性を持つACE阻害剤が,不血症の条件で治療的血管新生を助ける可能性があることを示唆しています.
科学分野:
- 血管生物学 血管生物学
- 薬理学 薬理学とは
背景:
- 内皮細胞 (ECs) は,産後血管新生に不可欠です.
- アンジオテンシン変換酵素 (ACE) 阻害剤は,内皮機能を改善する可能性があります.
研究 の 目的:
- ACE阻害剤キナプリラットが血管新生をインビボで促進するかどうかを調査する.
- キナプリラトの効果をカプトプリルと血管内皮成長因子 (VEGF) と比較する.
主な方法:
- 後肢イシュケミアのウサギモデルを使用した.
- ウサギは,キナプリラット,カプトプリル,再結合ヒトVEGF (rhVEGF),または治療を受けなかった.
- 血管新生は,血圧,血管活性,抵抗,血管撮影,毛細血管密度によって評価されました.
主要な成果:
- クィナプリラットは,rhVEGFに匹敵し,カプトプリルまたは対照群に優れている,血管新生を大幅に増加させた.
- キナプリラットは,カプトプリルとは異なり,組織のACE活性を効果的に低下させた.
- 機能的および形態学的アウトカムは,クイナプリラトで治療されたウサギの強化された血管新生をサポートしました.
結論:
- クイナプリラトによるACE阻害は,不血性後肢における血管新生を促進する.
- 高組織親和性を持つノンスルフヒドリルACE阻害剤は,治療的な血管新生に有益である可能性があります.
- 肌動脈不全症におけるACE阻害の利点には,付随的な発達が強化される可能性があります.
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