Mediation of vascular relaxation in epineurial arterioles of the sciatic nerve: Effect of diabetes in type 1 and type 2 diabetic rat models

Previously, the authors have reported that acetylcholine-induced vascular relaxation in epineurial arterioles of the sciatic nerve is mediated by nitric oxide (NO) and endothelium-derived hyperpolarizing factor (EDHF). Furthermore, they have demonstrated that acetylcholine-induced vasodilation in these vessels is impaired in streptozotocin-induced (type 1) and ZDF obese (type 2) diabetic rats. In the present study, the authors sought to determine the effect of diabetes on NO- and EDHF-mediated vasodilation in epineurial arterioles. In epineurial arterioles from nondiabetic Sprague-Dawley rats, NO and EDHF are equivalent in regard to their contribution to acetylcholine-induced vascular relaxation. In contrast, NO accounts for a greater portion of acetylcholine-induced vascular relaxation in normal glycemic ZDF lean rats. Following 4 weeks of hyperglycemia, the EDHF component of acetylcholine-induced vascular relaxation was totally inhibited in both streptozotocin-induced and ZDF obese diabetic rats. Vasodilation mediated by NO was still active in epineurial arterioles from both type 1 and type 2 diabetic rat models. These data suggest that diabetes causes an impairment in EDHF-mediated vascular relaxation and that interventions directed at improving EDHF production or bioactivity may improve vascular function in epineurial arterioles in diabetes.