In these conditions, the effects of insulin are mediated by an endothelial dysfunction explained in part, by the increased production of endothelin-1 (ET-1) which promotes vasoconstriction, oxidative stress, cell-growth and mitogenesis, and by the activation of the vascular tissue renin–angiotensin system (RAS) [87,88]. Here, EDN1 is linked to endothelial dysfunction.