Prieto-Carrasquero Minolfa C, Botros Fady T, Kobori Hiroyuki, Navar L Gabriel
Department of Physiology and Tulane Renal Hypertension Center, Tulane University, School of Medicine, New Orleans, LA, 70112.
J Am Soc Hypertens. 2009 Mar-Apr;3(2):96-104. doi: 10.1016/j.jash.2008.11.003.
Recently, the focus of interest on the role of the renin angiotensin system in the pathophysiology of hypertension has shifted towards greater emphasis on new developments in local renin angiotensin systems in specific tissues. We have focused our recent investigations on the role of the intrarenal-intratubular RAS in hypertension. All of the components needed for angiotensin II generation are present within the various compartments in the kidney. This brief review is focused on recent evidence that inappropriate activation of renin in distal nephron segments, by acting on angiotensinogen generated in the proximal tubule cells and delivered to the distal nephron may contribute to increased distal intrarenal angiotensin II formation, sodium retention and development and progression of hypertension.
最近，肾素血管紧张素系统在高血压病理生理学中作用的研究重点已转向更加强调特定组织中局部肾素血管紧张素系统的新进展。我们最近的研究集中在肾内肾小管内肾素血管紧张素系统在高血压中的作用。肾内生成血管紧张素II所需的所有成分都存在于肾脏的各个腔室中。本简要综述聚焦于近期的证据，即远端肾单位节段中肾素的不适当激活，通过作用于近端小管细胞产生并输送至远端肾单位的血管紧张素原，可能导致远端肾内血管紧张素II生成增加、钠潴留以及高血压的发生和进展。
