抑制 ангиотензин转化酶增加了通过内源性布拉迪基宁因通过人血管组织类型的塑原激活剂释放
Mias Pretorius1, David Rosenbaum, Douglas E Vaughan
1Department of Anesthesiology, Vanderbilt University Medical Center, Nashville, Tenn 37232-6602, USA.
Circulation
|February 5, 2003
概括
抑制 ангиотензин转化酶 (ACE) 会促进组织类型等离子素激活剂 (t-PA) 的释放. 这通过内源勃拉迪基宁发生,增强吸烟者的内皮t-PA释放.
科学领域:
- 心血管研究研究心血管研究
- 药理学 药理学 是一个学科.
- 内皮细胞功能 内皮细胞功能
背景情况:
- 抑制 ангиотензин转化酶 (ACE) 增强了对外源勃拉迪基宁的反应.
- 通过ACE抑制剂影响内皮功能的精确机制需要进一步阐明.
研究的目的:
- 测试该假设,即ACE抑制通过内源性布拉迪基宁增加内皮组织类型等离子素激活剂 (t-PA) 释放.
- 调查布拉迪基宁在调解ACE抑制剂对t-PA释放的影响中的作用.
主要方法:
- 在24名吸烟者中,静脉内给予埃纳拉普利拉特.
- 测量前臂血流 (FBF) 和净t-PA释放.
- 布拉迪基宁和甲胆在恩拉普利拉特前和期间的输液.
- 使用布拉迪基宁受体抗剂HOE 140或载体.
主要成果:
- 恩拉普里拉特显著增加了静止净t-PA释放,这一效应被HOE 140取消了.
- 抑制ACE增强了FBF和t-PA对外源勃拉迪基宁的反应.
- 埃纳拉普利拉特对t-PA释放的强化明显大于FBF的强化.
结论:
- 抑制ACE会增加构成性内皮t-PA的释放.
- 这种效果是通过内源勃拉迪基尼尼调节的.
- 布拉迪基宁在调解ACE抑制剂诱导的t-PA释放方面发挥着至关重要的作用.
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