A number of factors including hyperglycaemia, hypertension, dyslipidaemia and oxidative stress contribute to the development of vascular disease in diabetes, the chief cause of the increased morbidity and mortality associated with this disease. Within the vessel wall impairment of endothelial and smooth muscle responses both contribute to functional abnormalities such as reduced vasodilation and it has been shown that hypertension and diabetes have additive effects on vascular cell function. The development of structural changes such as atheromae involves, inter alia, the movement of smooth muscle cells from the tunica media to the subendothelial space, and the recruitment of endothelial cells and macrophages. At an intracellular level, some but not all the signalling pathways activated by hyperglycaemia and hypertension are fully known. In the case of hypertension there are both hormonal and cell stretch components involved in cell activation. In diabetes insulin resistance, high levels of glucose, the presence of advanced glycation end-products and intracellular oxidative stress can all contribute to abnormal cell responses. A fuller understanding of the signalling pathways involved may lead to the development of additional therapies for the prevention or reduction of vascular disease in diabetes.