Abstract
BACKGROUND: Depression contributes significantly to global burden of disease. Current traditional antidepressants focus on monoamine theory of depression, but the treatment effect is not satisfactory. It is worthy to explore other mechanisms, which may contribute to the treatment of depression. Preclinical and epidemiological studies show the potential role of the renin-angiotensin system (RAS) in treatment of depression. Some clinical studies also showed the role of angiotensin converting enzyme (ACE) genetic polymorphisms in antidepressant treatment response. Until now, no study evaluates the changes of components of the RAS in patients with major depressive disorder (MDD). AIMS & OBJECTIVES: The study aims to compare RAS markers between patients with MDD and healthy controls, and the changes of RAS markers after 2-month antidepressant treatment in patients with MDD. METHOD: We recruited 42 drug-free patients with MDD and 35 healthy controls. Among 42 patients with MDD, 22 were followed for 2 months. Each patient with MDD were followed three times, i.e. baseline, the first follow-up (around 4 week), and the second follow-up (around 8 week). We used Montgomery-Asberg Depression Rating Scale (MADRS) and Depression and Somatic symptoms Scale to assess the severity of depression, and evaluate serum levels of RAS markers, such as ACE2, Angiotensin II (Ang II), and Angiotensin 1-7 (Ang 1-7). RESULTS: There were no differences in mean age and the distribution of sex between patients with MDD and healthy control. Serum levels of ACE2, Ang II, and Ang 1-7 did not differ between patients and healthy control. In addiction, we did not find any changes of serum levels of ACE2, Ang II, and Ang 1-7 after 2 months antidepressant treatment. Furthermore, there were no differences in these RAS markers between patients with good response and without good response after 2 months antidepressant treatment. DISCUSSION & CONCLUSIONS: Small sample size is a major limitation in our study. However, from our study results, the RAS may not play a significant role in psychophysiology and treatment response in patients with MDD.