Investigation on the vasodilatory effect of insulin through KATP channels and NO pathway in the skin vessels of native and diabetic rats

Introduction: Endothelium and smooth muscle dysfunction are the most important complications of diabetes. In type 1 diabetic patients, absence of insulin leads to vasoconstriction and lower skin blood perfusion. Release of some mediators by endothelium which is induced by insulin causes vasodilation, but the exact mechanism of insulin vasodilatory effect is not detected properly. At present study we investigated the role of NO as a vasodilator and KATP channels and their intraction in the vasodilatory effect of insulin on the skin vessles. Methods: Male wistar rats (200-250 gr) were made diabetic by streptozocin (50mg/kg, s.c). After 40 days of diabetes induction, skin blood flow was measured by Laser Doppler Flowmetry technique (LDF). Insulin, LNNA (NO blocker) and Glibenclamide (KATP blocker) infusion were made by infusion pump subcutaneousely. Results: 1- Insulin increases skin blood flow in both control and diabetic groups and this increase was significantly higher in diabetic group. 2- Insulin vasodilatory effect was decreased by LNNA. 3- The vasodilatory effect of insulin was decreased by Glibenclamide. 4- Simultaneous block of both NO and KATP was more effective. Conclusion: Insulin induces vasodilation in part by NO release and partly by activation of K ATP channels. However some interaction has been seen between both routes. Although by block of both these routes, blood flow has not been completely inhibited. So it is supposed that other factors may be involved in this effect and yet to be illucidated.