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Captopril inhibits glucose accumulation in retinal cells in diabetes.

PURPOSE
Clinical studies have detected an unexpected inhibition of diabetic retinopathy by angiotensin-converting enzyme (ACE) inhibitors, but the mechanism for this action is unclear. In light of evidence indicating that the severity of hyperglycemia is a major initiating factor in the pathogenesis of the retinopathy, this study was conducted to examine the effect of ACE inhibitors on glucose accumulation in retinas of diabetic rats.


METHODS
Rats were made experimentally diabetic by injection of streptozotocin and treated with captopril (25 mg/kg body weight per day) or atenolol (10 mg/kg body weight per day) for 8 weeks. Bovine retinal endothelial cells were cultured in medium containing either 5.5 or 25 mM glucose and treated with different concentrations of captopril or lisinopril for 5 days. Glucose content in retinas and cultured cells was measured by spectrometry. Expression of glucose transporter (GLUT)-1 in retinas and cultured cells was determined by Western blot analysis. Glucose uptake was performed by using 3-O-methyl-D-[(3)H] glucose.


RESULTS
Treatment of rats with captopril inhibited the diabetes-induced accumulation of glucose in the retina by 48% (P < 0.01) compared with the diabetic control, but atenolol had no significant effect. Similarly, captopril and lisinopril significantly inhibited intracellular accumulation of glucose in primary bovine retinal endothelial cells cultured in an elevated glucose concentration. These data indicate that the captopril-induced inhibition of glucose accumulation observed in retinal tissue of diabetic rats was not due to reduction in blood pressure or in vascular permeability. Although it had no effect on the expression of the GLUT1 in retinas and cultured retinal endothelial cells, captopril at a concentration of 2 mM significantly inhibited the high-glucose-induced increase in GLUT1-mediated glucose transport in cultured retinal endothelial cells by 67% +/- 10%.


CONCLUSIONS
Inhibition of glucose accumulation within retinal cells probably contributes at least in part to the observed inhibition of diabetic retinopathy by ACE inhibitors.