Navar L Gabriel, Kobori Hiroyuki, Prieto-Carrasquero Minolfa
Department of Physiology SL39, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112, USA.
Curr Hypertens Rep. 2003 Apr;5(2):135-43. doi: 10.1007/s11906-003-0070-5.
Elevations in intrarenal angiotensin II (Ang II) cause reductions in renal function and sodium excretion that contribute 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 can be explained from 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 angiotensinogen (AGT) mRNA and protein. The increased intrarenal AGT production is associated with increased intrarenal and intracellular Ang II contents and urinary AGT excretion rates. The increased urinary AGT indicates spillover of AGT into distal nephron segments supporting enhanced 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.
肾内血管紧张素II（Ang II）水平升高会导致肾功能和钠排泄减少，这会促使高血压病情进展并导致肾和血管损伤。肾内Ang II通过多种过程增加，导致其水平远高于循环水平所能解释的程度。在依赖Ang II的高血压中，Ang II通过AT1受体机制内化，但肾内也持续产生Ang II。Ang II对肾内血管紧张素原（AGT）的mRNA和蛋白质发挥正反馈作用。肾内AGT生成增加与肾内和细胞内Ang II含量增加以及尿AGT排泄率升高有关。尿AGT增加表明AGT溢出到远端肾单位节段，支持远端Ang II形成增加和钠重吸收。肾内Ang II的增加为对肾功能、钠排泄和高血压维持的持续作用提供了基础。
