Diabetes mellitus is an important risk factor for cardiovascular disease and hyperglycaemia is being more and more acknowledged as a mediator of vessel damage. It is becoming increasingly clear that hyperglycaemia involves a number of different parameters (acute, chronic, and post-prandial hyperglycaemia), all of which contribute to the vascular damage caused by high glucose levels. High glucose levels are associated with the non-enzymatic glycation of both extra- and intracellular proteins, the accumulation of sorbitol via the aldose-reductase pathway, the activation of protein kinase C isoforms, and the reduced bioavailability of nitric oxide. The generation of reactive oxygen species may be a common downstream mechanism by means of which the multiple by-products of glucose exert their adverse effects on blood vessels.