Cardiovascular complication contributes an important role to morbidity and mortality in patients with diabetes. We hypothesized that these abnormalities are mainly mediated by oxidative stress, endothelial dysfunction and impaired intracellular communications. Thus, we examined vasoactivity and expression of connexin (Cx) 43 and 40, protein kinase C-ɛ (PKCɛ) and NADPH oxidase of the vasculature of thoracic aorta in streptozotocin (STZ)-injected rats, and whether NaHS could reverse these abnormalities compared with aminoguanidine.

Male Sprague–Dawley rats were administered with STZ (60 mg/kg, i.p.) to induce diabetes. Diabetic rats were divided into untreated and treated groups in the 5th–8th week and intervention with either NaHS (5 mg/kg daily, s.c.) or aminoguanidine (100 mg/kg daily, p.o.) was made.

In rats with untreated diabetes, hyperglycaemia, increased activity of inducible nitric oxide (NO) synthase, increased NO, mild vascular spasm, reduced NO bioavailability and diminished vasorelaxation were found. These findings were accompanied by downregulated Cx43 and Cx40, and upregulated PKCɛ and NADPH oxidase subunits p22^phox/p47^phox/p67^phox in the thoracic aorta. NaHS appears to be as effective as aminoguanidine in attenuating these abnormalities.

NaHS shows promise in relieving diabetic vascular abnormality by upregulating junctional connexin Cx40 and Cx43, via normalizing NADPH oxidase and PKCɛ in the vasculature.