The mean plasma norepinephrine and epinephrine concentrations with the patients in the supine position and after 2,5 and 10 minutes of standing (hereafter referred to as "supine" and "standing" plasma norepinephrine or epinephrine levels) in 100 nonketotic diabetic patients were not significantly different from those in normal subjects indicating that alterations in sympathetic neural and adrenomedullary net secretory activity are not a feature of diabetes mellitus per se. Alterations of plasma catecholamine levels were not a consistent feature of diabetic peripheral neuropathy, retinopathy or nephropathy except that the levels of both norepinephrine and epinephrine were low in patients with nephrotic proteinuria, perhaps reflecting diminished plasma protein binding. Plasma catecholamine concentrations in patients receiving long-term therapy with insulin or oral hypoglycemic agents were not different from those in patients receiving no drug therapy or from those in normal subjects. Abnormalities in adrenergic physiology were identified in 26 per cent of the diabetic patients. Seven patients had postural hypotension with a blunted plasma norepinephrine response to standing. These patients with hypoadrenergic postural hypotension have diabetic adrenergic neuropathy. Eleven patients had increased standing plasma norepinephrine concentrations (peak values ranging from 960 to 9,310 pg/ml); seven of these also had elevated supine plasma norepinephrine levels (421 to 816 pg/ml). Three of these patients exhibited postural hypotension (standing decrements in mean blood pressure ranging from 20 to 83 mm Hg) and represent a newly recognized clinical syndrome of hyperadrenergic postural hypotension. It is suggested that diabetic patients exhibiting this hyperadrenergic pattern have vascular resistance endogenous norepinephrine. Eight patients had postural hypotension with normal plasma norepinephrine concentrations perhaps reflecting combined norepinephrine resistance and partial adrenergic neuropathy.