Augustin M, Dumitriu L, Popovici D, Gabrielescu-Berceanu A, Ioaniţiu D, Mănciulescu D, Marinescu I, Tache A, Cristoveanu A, Pop A, Mazilu M, Stefănescu A M, Giurcăneanu M, Olaru A, Paţachi M, Ionescu V, Dinulescu E
Endocrinologie. 1983 Jan-Mar;21(1):43-9.
The authors have studied on 25 cases of hypercorticism, one of the mechanisms of producing arterial hypertension, the renin-angiotensin system. The study showed that in only 20% of the cases plasma renin activity was high whereas in the remaining 80% other mechanisms were responsible for the hypertension. In the cases in which the plasma activity of renin was high, by studying the changes in the value of electrolytes we were able to derive some understanding of the mechanism of action of the RA2A system. Thus, the literature data show that sometimes the excess of glucocorticoids causes hypertension by activating directly the RA2A system and concomitently inhibiting the renin-kalikrein system (RKKS) and PgS; at other times, the excess of glucocorticoids is exerted on the same renin-angiotensin system, but via ACTH and ADH, the electrolytes values being those that demonstrate the borrowed mechanism.
作者研究了25例皮质醇增多症患者，这是产生动脉高血压的机制之一，即肾素-血管紧张素系统。研究表明，仅20%的病例血浆肾素活性升高，而其余80%的高血压由其他机制引起。在血浆肾素活性升高的病例中，通过研究电解质值的变化，我们对RA2A系统的作用机制有了一些了解。因此，文献数据表明，有时糖皮质激素过量通过直接激活RA2A系统并同时抑制肾素-激肽释放酶系统（RKKS）和PgS来导致高血压；在其他时候，糖皮质激素过量作用于同一肾素-血管紧张素系统，但通过促肾上腺皮质激素（ACTH）和抗利尿激素（ADH），电解质值显示出这种间接机制。
