洛萨坦在高血压人群中增加了布拉迪基宁水平
Duncan J Campbell1, Henry Krum, Murray D Esler
1St Vincent's Institute of Medical Research, 41 Victoria Parade, Fitzroy, Victoria 3065, Australia. dcampbell@svi.edu.au
Circulation
|January 19, 2005
概括
血管素1型受体抑制剂,如洛萨坦,在高血压患者中增加布拉迪基宁水平. 这可能有助于它们的治疗效果和副作用,如血管.
科学领域:
- 心血管药理学心血管药理学
- 高血压研究 高血压研究
- 脏生理学 脏生理学
背景情况:
- ангиотензин 1 型 (AT1) 受体抑制剂用于治疗高血压.
- 动物和人类研究表明,金因在AT1受体阻断剂作用中起作用.
- AT1受体阻塞剂对人体基宁水平的影响尚不清楚.
研究的目的:
- 为了研究洛萨坦和埃普萨坦对人类基本高血压的基因和血管素水平的影响.
- 探索AT1受体阻断剂诱导的形状变化背后的潜在机制.
主要方法:
- 一个双盲,3期,3疗法交叉试验,涉及患有基本高血压的患者.
- 使用安慰剂,洛萨坦 (50毫克每日一次) 和埃普罗萨坦 (600毫克每日一次).
- 在动脉血液中测量血管素 (Ang),布拉迪基宁 (BK) 和卡利丁,使用基于HPLC的放射性免疫检测.
主要成果:
- 洛萨坦显著增加了血中的布拉迪基宁 (BK) 水平 (2倍),并将BK-1-7/BK-1-9比率降低了55%.
- 沙坦呈现了类似的布拉迪基宁水平变化的趋势;卡利丁水平保持不变.
- 这两种药物都增加了Ang I,Ang II和Ang- 2-8的水平,而eprosartan也增加了Ang-3-8).
- 观察到Ang-II/Ang I和Ang-{1-7) /Ang I比率显著降低,而血ACE活性没有受到影响.
结论:
- 洛萨坦可明显增加高血压患者的布拉迪基宁水平.
- 通过ACE和中性内酶降低的新陈代谢可能会导致勃拉迪基宁水平升高.
- 勃拉迪基宁的增加可能是AT1受体抑制剂的类效应,调解治疗作用和潜在的血管副作用.
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