Increased nitric oxide activity compensates for increased oxidative stress to maintain endothelial function in rat aorta in early type 1 diabetes

Hyperglycaemia and oxidative stress are known to acutely cause endothelial dysfunction in vitro, but in the initial stages of diabetes, endothelium-dependent relaxation is preserved. The aim of this study was to investigate how endothelium-dependent relaxation is maintained in the early stages of type 1 diabetes. Diabetes was induced in Sprague-Dawley rats with a single injection of streptozotocin (48 mg/kg, i.v.), and after 6 weeks, endothelium-dependent and endothelium-independent relaxations were examined in the thoracic aorta in vitro. Lucigenin-enhanced chemiluminescence was used to measure superoxide generation from the aorta. Diabetes increased superoxide generation by the aorta (2,180 +/- 363 vs 986 +/- 163 AU/mg dry tissue weight).