Purchase this article with an account.
H. Sánchez–Tocino, M.I. López Gálvez, M. Jarrín–Jarrín, M.A. Saornil, J.C. Pastor–Jimeno; Upregulation of the Vascular Endothelial Growth Factor by an Angiotensin Converting Enzyme Inhibitor in Streptozotocin–Diabetic Rats . Invest. Ophthalmol. Vis. Sci. 2005;46(13):434.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
Purpose: Recently the EUCLID study group reported that a Angiotensin converting enzyme inhibitor (ACEI) treatment was associated with a reduction in diabetic retinopathy (DR) progression and in proliferative diabetic retinopathy, providing a potential clinical role for suppression of the renin–angiotensin system (RAS) in preventing and treating retinal neovascularization. However we do not know if the effect of ACEI on vascular permeability was due to a reduction in systemic blood pressure or a specific effect on the RAS. Methods: Diabetes was induced by intraperitoneal injection of streptozotocin in 60 male wistar rats. 10 rats no induced were used as control, nondiabetic group. Diabetic rats were divided in two groups: diabetic rats treated with ACEI (captopril 10 mg/Kg, starting at the 4 th month until 11–month duration of diabetes) and diabetic rats without ACEI. Vascular endothelial growth factor (VEGF) protein in retina and retinal pigment epithelium (RPE) homogenates by assessed sandwich ELISA were measured in the right eye. The left eye was used to localize VEGF protein by immunohistochemistry studies; retinal transections were examined by light microscopy. Results: There was extensive gliosis and disruption of retinal layers in diabetic rats compared with nondiabetic rats. VEGF protein concentration (means ± SD) was increased in diabetic rats compared with nondiabetic ones (55,06 ± 35,33 vs. 30,70 ± 16; p = 0.017) in RPE. There were not significant statistical differences in levels of VEGF in retina between diabetic and nondiabetic rats (30.26 ± 23.22 vs. 17.69 ± 9.3; p= 0.143 ). Treatment with captopril does not have any different effect on VEGF protein levels in treated with IECA versus without IECA diabetic rats in retina (35.06 ± 31.5 vs. 25,47 ± 9.5; p = 0.902) or in RPE ( 53.15 ± 133 vs. 56.97 ± 49.5 ; p =0.19). The localization of VEGF in the retina was not altered in animals with experimental diabetes, but increased levels were detected in diabetic rats. Captopril do not modify diabetes associated changes in VEGF protein. Conclusions: These data obtained from a rodent model support the findings already reported of a physiologic role for VEGF in the retina and the RPE. The changes in retinal detection of VEGF protein in association with diabetes suggest a role for this pathway in DR. Captopril do not modify regulation of VEGF protein in the retina during early DR.
This PDF is available to Subscribers Only