Suppression of sodium-dependent glucose uptake by captopril improves high-glucose-induced morphological and functional changes of cultured bovine retinal pericytes.

The effects of captopril on glucose uptake, as well as morphological and functional changes of retinal pericytes, in a high-glucose medium were examined. Retinal pericytes were incubated in medium with 5 and 30 mM glucose and 30 mM glucose with 10(-6) to 10(-3) M captopril. Captopril decreased the cellular uptakes of d-glucose and alpha-methyl glucoside in the presence, but not in the absence, of sodium. The cellular size and contents of glucose, sorbitol, and fructose were increased in 30 mM glucose concomitant with the decreased thymidine, cellular DNA content, and ratios in glucose to sorbitol and to fructose, compared with those in 5 mM glucose. These changes observed in 30 mM glucose were reversed by 10(-4) M captopril. These data suggest that the suppression of d-glucose uptake through a sodium-coupled glucose transporter by captopril may attenuate the swelling and loss of pericytes observed in the early stage of diabetic retinopathy.