Type 1 diabetes is commonly associated with microvascular complications. Most of the microvascular blood vessels are involved but those in the kidney, retina and large nerves exhibit the more significant pathology. Haemodynamic and metabolic factors both alone and through the activation of a common pathway contribute to the characteristic dysfunction observed in diabetic vasculopathy. The haemodynamic abnormalities in type 1 diabetes are characterized by increased systemic blood pressure and altered blood flow with subsequent activation of various vasoactive factors, which can contribute to the maintenance of the haemodynamic alterations and to the development and progression of the microvascular complications. These vasoactive factors include vasoconstrictors such as angiotensin II, and endothelin, as well as vasodilators such as nitric oxide (NO). Systemic hypertension and vasoactive factors independently and in interaction with the metabolic pathway activate intracellular second messengers, nuclear transcription factors and various growth factors which lead to the typical functional and structural alterations of diabetic microvascular complications. Therapeutic strategies involved in the management and prevention of diabetic complications currently include antihypertensive agents, particularly those that interrupt the renin-angiotensin system. Further understanding of the interactions among the vasoactive factors, the intracellular second messengers and the growth factors may help to identify novel strategies to influence the action of the vasoactive factors. These novel therapies, together with specific inhibitors of the metabolic pathway or the common pathway, may provide the possibility of preventing or even reversing the progression of diabetic microvascular complications.
