有证据表明,氨酸- ангиотензин系统在酸盐耐受性方面的因果作用
1Department of Medicine, Emory University School of Medicine, Veterans Administration Hospital, Atlanta, GA, USA.
Circulation
|June 22, 1999
概括
耐受性酸甘 (NTG) 治疗与血管超氧化物产生增加有关,由血管新生素II和内甲蛋白-1通路驱动. 阻止这些通路可以防止耐受性,并恢复NTG的有效性.
科学领域:
- 心血管药理学心血管药理学
- 血管生物学 血管生物学
- 酸盐耐受性机制
背景情况:
- 酸甘油 (NTG) 治疗增加了血管内甲蛋白-1 (ET-1) 和超氧化物 (O2.-) 的产生,可能是通过血管新生素II.
- 在早期NTG疗法期间,氨酸-血管酶系统被激活.
- 假设:在NTG治疗期间, ангиотензинII或ET-1会增加血管O2的产生.
研究的目的:
- 调查血管素II和ET-1在酸盐耐受性发展中的作用.
- 确定NTG疗法对血管O2-生产和氨酸-血管新生素系统的影响.
- 评估AT1和ET-1受体阻断在预防NTG耐受性的有效性.
主要方法:
- 新西兰白用NTG贴片治疗了3天.
- 评估了血雷宁活性,AT1受体表达,血管ACE活性和NTG血管扩张功效.
- 测量了使用素增强化学发光的血管O2-生产.
- 服用AT1受体对抗剂洛萨坦和ET-1受体阻断剂博森坦.
主要成果:
- 治疗NTG增加了血内活性和血管O2-生产,导致NTG放松 (耐受性) 减弱.
- 耐受性与增加的AT1受体mRNA和ACE活性有关.
- 洛萨坦剂量取决于正常化的O2生产,防止NTG耐受性和交叉耐受性.
- 博森坦也表现出类似的效果,但效果不那么明显.
结论:
- ангиотензин II 在酸盐耐受性发展中起着显著的病理生理作用.
- 恩多林-1有助于酸盐耐受性,尽管比血管新生素II的作用要小.
- 在NTG治疗期间,AT1和ET-1受体阻断对耐受性和O2-产生产生积极影响.
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