One of the earliest manifestations of diabetic neuropathy is denervation of the cardiovascular system; loss of heart rate variability may have a prevalence as high as 21.5% in diabetic patients, and declines at 1 beat/min/year, which is 3 times faster than in normal subjects. The cause of this neuropathy is unknown: attempts at decreasing the excess quantities of sorbitol, glucose and fructose in nerve tissue have lead to little functional improvement in man. Nerve ischaemia and immunological damage have stimulated increased interest lately, the latter particularly because of the structural homology of nerve growth factor and insulin. Symptoms from autonomic neuropathy are rare. When present they may well be intermittent, but never remit; they rarely progress or become disabling. One uncommon consequente of loss of sympathetic vascular tone is postural hypotension. This may result from failure of splanchnic vasoconstriction on standing. Food and insulin can greatly exacerbate the postural blood pressure fall. Reduced vascular tone in the neuropathic foot leads to increased arterio-venous shunt flow. The local reflex control of this shunt flow is also abnormal: paradoxical vasoconstriction occurs in response to local skin heating and postural reflexes are reduced. This high shunt flow together with its abnormal vascular control may be important in the pathogenesis of neuroarthropathy and foot ulceration. The prognosis of patients with autonomic neuropathy is better than previously reported. Abnormal heart rate variability alone is of no prognostic value. The presence of symptoms, in particular postural hypotension, significantly reduces survival. The majority of deaths however, result from concurrent renal disease and macrovessel atheroma.