Swales J D, Samani N J
Department of Medicine, Leicester Royal Infirmary, UK.
J Hum Hypertens. 1993 Aug;7 Suppl 2:S3-6.
Biochemical and bioassay evidence has proved the existence of tissue RAA systems although their function has not been satisfactorily defined. There are two sources of tissue renin: uptake from plasma and local synthesis. The uptake system has been demonstrated in arterial tissue. Retention of renin can be demonstrated in the aortic wall and the presence of renin at this site is closely correlated with the persistent elevation of blood pressure. Renin gene expression can be demonstrated in several organs such as the liver, brain and arterial wall, although the function of renin or pro-renin at these sites is unknown. Intracellular angiotensin II receptors have been identified that play a role in regulating gene expression. In addition to raising vascular tone, angiotensin II generated in this way could have a trophic action upon cardiac and vascular structures. There is now very strong evidence in favour of the extrarenal RAA system having a pathogenetic role in some forms of hypertension. Renin gene polymorphisms co-segregate with blood pressure in some genetic models, despite normal or low plasma renin and incorporation of an additional mouse renin gene construct into the rat genome produces severe hypertension despite suppression of renal renin.
生化和生物测定证据已证明组织肾素-血管紧张素-醛固酮系统（RAA系统）的存在，尽管其功能尚未得到令人满意的界定。组织肾素的来源有两个：从血浆摄取和局部合成。摄取系统已在动脉组织中得到证实。肾素可在主动脉壁中潴留，且该部位肾素的存在与血压持续升高密切相关。肾素基因表达可在肝脏、大脑和动脉壁等多个器官中得到证实，尽管这些部位肾素或肾素原的功能尚不清楚。已鉴定出细胞内血管紧张素II受体，其在调节基因表达中发挥作用。除了升高血管张力外，以这种方式产生的血管紧张素II可能对心脏和血管结构具有营养作用。现在有非常有力的证据支持肾外RAA系统在某些形式的高血压中具有致病作用。在一些遗传模型中，肾素基因多态性与血压共分离，尽管血浆肾素正常或偏低，并且将额外的小鼠肾素基因构建体导入大鼠基因组会导致严重高血压，尽管肾脏肾素受到抑制。
