Suzaki Yuki, Prieto-Carrasquero Minolfa C, Kobori Hiroyuki
Department of Physiology, and Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, New Orleans, LA, USA.
Curr Hypertens Rev. 2006;2(2):151-157. doi: 10.2174/157340206776877325.
It is well recognized that the renin-angiotensin system plays an important role in the regulation of arterial pressure and sodium homeostasis. Recent years, many studies have shown that local tissue angiotensin II levels are differentially regulated and cannot be explained on the basis of circulating concentrations. All of the components needed for angiotensin II generation are present within the various compartments in the kidney including the renal interstitium and the tubular network. The cascade of the renin-angiotensin system demonstrates three major possible sites for the pharmacological interruption of the renin-angiotensin system: the interaction of renin with its substrate, angiotensinogen, the angiotensin converting enzyme, and angiotensin II type 1 receptors. This brief article will focus on the role of the intratubular renin-angiotensin system in the pathophysiology of hypertension and the responses to the renin-angiotensin system blockade by renin inhibitors, angiotensin converting enzyme inhibitors and angiotensin II type 1 receptor blockers.
众所周知,肾素 - 血管紧张素系统在动脉血压调节和钠稳态中发挥着重要作用。近年来,许多研究表明,局部组织中的血管紧张素II水平受到不同调节,无法根据循环浓度来解释。血管紧张素II生成所需的所有成分都存在于肾脏的各个区域内,包括肾间质和肾小管网络。肾素 - 血管紧张素系统的级联反应显示了肾素 - 血管紧张素系统药理学阻断的三个主要可能位点:肾素与其底物血管紧张素原的相互作用、血管紧张素转换酶以及血管紧张素II 1型受体。这篇简短的文章将重点关注肾小管内肾素 - 血管紧张素系统在高血压病理生理学中的作用以及肾素抑制剂、血管紧张素转换酶抑制剂和血管紧张素II 1型受体阻滞剂对肾素 - 血管紧张素系统阻断的反应。