Coezy E, Bouhnik J, Clauser E, Pinet F, Philippe M, Menard J, Corvol P
In Vitro. 1984 Jul;20(7):528-34. doi: 10.1007/BF02639768.
Angiotensinogen is synthesized in large amounts by Fao cells derived from the Reuber H35 rat hepatoma in a medium enriched with 5% fetal bovine serum (FBS). Treatment of FBS with dextran-coated charcoal removed endogenous steroids without modifying angiotensinogen production. This treatment allowed the study of the effects of steroids on angiotensinogen production. Hydrocortisone increased the angiotensinogen synthesis in a dose-dependent manner. The antiglucocorticoid RU 38486 did not change the basal rate of angiotensinogen production but inhibited the stimulation by hydrocortisone. Similar results were obtained with dexamethasone. Angiotensinogen biosynthesis seems to be regulated by two distinct mechanisms: (a) glucocorticoid independent, controlling the basal rate of angiotensinogen production and (b) glucocorticoid dependent, mediating the increased rate of angiotensinogen production upon glucocorticoid treatment.
血管紧张素原由源自鲁伯H35大鼠肝癌的Fao细胞在富含5%胎牛血清（FBS）的培养基中大量合成。用葡聚糖包被的活性炭处理FBS可去除内源性类固醇，而不改变血管紧张素原的产生。这种处理使得能够研究类固醇对血管紧张素原产生的影响。氢化可的松以剂量依赖性方式增加血管紧张素原的合成。抗糖皮质激素RU 38486不会改变血管紧张素原产生的基础速率，但会抑制氢化可的松的刺激作用。地塞米松也得到了类似的结果。血管紧张素原的生物合成似乎受两种不同机制调节：（a）不依赖糖皮质激素，控制血管紧张素原产生的基础速率；（b）依赖糖皮质激素，介导糖皮质激素处理后血管紧张素原产生速率的增加。
