激活的组织肾素-血管紧张素系统会加重心力衰竭的进展。
Activated tissue renin-angiotensin systems add to the progression of heart failure.
作者信息
Pinto Y M, Buikema H, van Gilst W H, Lie K I
机构信息
Dept. of Cardiology, University of Groningen, The Netherlands.
出版信息
Basic Res Cardiol. 1996;91 Suppl 2:85-90. doi: 10.1007/BF00795368.
In this paper, we review the hypothesis that activated tissue renin-angiotensin systems play a detrimental role in heart failure. The main arguments for this idea are discussed: a) tissue renin-angiotensin systems behave functionally distinct from the circulating renin-angiotensin system; b) tissue renin-angiotensin systems are activated in heart failure; c) activated tissue renin-angiotensin systems induce cardiovascular dysfunction. Finally, this hypothesis predicts that optimal treatment in heart failure requires the inhibition of tissue renin-angiotensin systems. However, studies pertaining to this prediction are still lacking, particularly in human subjects.
在本文中，我们回顾了激活的组织肾素 - 血管紧张素系统在心力衰竭中起有害作用这一假说。讨论了支持这一观点的主要论据：a）组织肾素 - 血管紧张素系统在功能上与循环肾素 - 血管紧张素系统不同；b）组织肾素 - 血管紧张素系统在心力衰竭中被激活；c）激活的组织肾素 - 血管紧张素系统会诱发心血管功能障碍。最后，这一假说预测，心力衰竭的最佳治疗需要抑制组织肾素 - 血管紧张素系统。然而，有关这一预测的研究仍然缺乏，尤其是在人类受试者中。
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