アンジオテンシン変換酵素の阻害は,内生的なブラジキニン経由でヒトの血管組織型のプラズミノゲン活性化剤の放出を増加させます
Mias Pretorius1, David Rosenbaum, Douglas E Vaughan
1Department of Anesthesiology, Vanderbilt University Medical Center, Nashville, Tenn 37232-6602, USA.
Circulation
|February 5, 2003
まとめ
アンジオテンシン変換酵素 (ACE) の阻害は,組織型プラズミノゲン活性化剤 (t-PA) の放出を促進します. これは,内在的なブラジキニンを介して発生し,喫煙者における内皮のt-PA放出を促進します.
科学分野:
- 心血管研究 循環器科の研究
- 薬理学 薬理学とは
- 内皮機能の機能について
背景:
- アンジオテンシン変換酵素 (ACE) の阻害は,外因的なブラジキニンに対する反応を高めます.
- ACE阻害剤が内皮機能に影響を与える正確なメカニズムについては,さらなる解明が必要である.
研究 の 目的:
- ACE阻害が内皮組織型プラズミノゲン活性化剤 (t-PA) の内生性ブラジキニンによる放出を増加させるという仮説を検証する.
- t-PA放出に対するACE阻害剤の作用を媒介するブラジキニンの役割を調査する.
主な方法:
- 24人の喫煙者に静脈内エナラプリラトを投与した.
- 前腕の血流量 (FBF) とt-PAの純放出量を測定する.
- ブラジキニンとメタコレンの注入は,エナラプリラト前およびその間に行われます.
- ブラジキニン受容体アンタゴニストHOE 140または媒体の使用.
主要な成果:
- エナラプリラトは,静止状態の純t-PAの放出を大幅に増加させ,HOE 140によって廃止された効果でした.
- ACEの阻害は,外因的なブラジキニンに対するFBFとt-PAの両方の反応を強めた.
- エナラプリラトによるt-PA放出の強化は,FBFの強化よりも著しく大きかった.
結論:
- ACEの阻害は,構成的な内皮のt-PAの放出を増加させます.
- この効果は内在的なブラジキニンによって媒介されます.
- ブラディキニンは,ACE阻害剤によって誘発されたt-PAの放出を媒介する上で重要な役割を果たします.
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