OBJECTIVE: To observe the changes in retina after traumatic brain injury (TBI), and the effect of Losartan, an angiotensin II receptor antagonist, which inhibits the vasoconstrictor and platelet aggregation. STUDY DESIGN: Male Sprague Dawley rats (n=30) were divided into 3 groups of 10: Control (isotonic saline solution given intragastrically for 7 days), Trauma (craniectomy under anesthesia, saline solution administered intragastrically, sacrificed after 7 days), and Trauma+Losartan (after craniotomy, 30 mg/kg losartan administered for 7 days, sacrificed at the end of the 7th day). Retina and blood samples were taken. MDA, GSHPx, and MPO were used as biochemical markers. Tissues were fixed in a 10% formalin solution and embedded in paraffin blocks for histopathologic examination; 5µmthick sections were obtained and stained with HE. RESULTS: MPO activity significantly decreased in the Trauma group after TBI as compared with Controls (p<0.001). The MDA level was low in the Losartan group (p<0.001). GSHPx levels in the Trauma group were lower than levels in Controls (p<0.001). Hypertrophy and intense chromatin were observed in some of the photoreceptors in the Trauma group. Dilation and endothelial hyperplasia were observed in the vessels towards the ganglion layer. In the Trauma+Losartan group a significant improvement was observed in the nuclei of the photoreceptors, and edema between the membranes disappeared. VEGF expression in the Trauma group was increased in pigment epithelium cells. In the Trauma+Losartan group VEGF expression was evident in the inner and outer limiting membranes in the pigment epithelium and ganglion cells. In the Control group there was negative expression in the distribution of APAF in the nuclei of the photoreceptors. In the Trauma group APAF1 positive expression in the limiting membrane with degenerative photoreceptors and an increase in APAF1 expression was observed. In the Trauma+Losartan group, APAF1 expression was negative in ganglion cells. CONCLUSION: Losartan plays a role in the development of mitotic activity and decrease of apoptotic process in preventing cell damage, and as it induces angiogenic development it can be an important prophylactic agent in vascular remodeling. © Science Printers and Publishers, Inc.