肾内血管紧张素2与高血压

肾内高水平的血管紧张素2(intrarenal angiotensinⅡ,AngⅡ)可引发肾功能下降和钠排出量降低,这在高血压的发生发展以及肾脏和血管的损伤中起重要作用。多种途径可导致肾内AngⅡ升高,且所升高的水平已远超过循环量水平。在AngⅡ依赖型高血压中,AngⅡ通过AT1受体机制内化,同时持续生成维持其水平。AngⅡ对肾内血管紧张素肽原(AGT)mRNA表达和蛋白水平有正反馈作用,而肾内AGT的升高与肾内AngⅡ含量及尿AGT排出率有关。尿AGT含量升高说明AGT溢至远端肾单位从而增强远端肾小管中AngⅡ的形成和对钠的重吸收。AngⅡ的增加为肾功能的维持、钠排泄、高血压的发展提供基础。

Intrarenal angiotenhsin II and hypertension

Elevations in intrarenal angiotensin Ⅱ (Ang Ⅱ)cause reductions in renal function and sodiumexcretion that con-tribute to progressive hypertension and lead to renal and vascular injury.Augmentation of intrarenal Ang Ⅱ occurs by several processes, leading to levels much greater than the circulating levels.In Ang Ⅱ-dependent hypertension,Ang Ⅱ is internalized via an AT1 receptor mechanism,but there is also sustained intrarenal production of Ang Ⅱ.Ang Ⅱ exerts a positive feedback action on intrarenal angio-tensinogen (AGT)mRNA and protein.The increased intrarenal AGT production is associated with increased intrarenal Ang Ⅱ contents and urinary AGT excretion rates.The increased urinary AGT indicates spillover of AGT into distal nephron segments supporting en-hanced distal Ang Ⅱ formation and sodium reabsorption.The augmentation of intrarenal Ang Ⅱ provides the basis for sustained actions on renal function,sodium excretion,and maintenance of hypertension.