SUMMARY High basal gastrin levels in pure autonomic failure could result from peripheral vagus nerve involvement, whereas the increased response during hypoglycaemia may reflect adrenergic supersensitivity. A reduced gastrin increment in multiple system atrophy was found following insulin-hypoglycaemia and is consistent with decreased gastrin release secondary to diminished central sympathetic nervous system activation in the absence of peripheral denervation supersensitivity.Chronic autonomic failure is attended by a variety of abnormal biochemical, pharmacological, and hormonal responses.' Although the symptoms of autonomic dysfunction are quite similar, central neurological signs such as ataxia, rigidity and bradykinesia distinguish patients who have multiple system atrophy with autonomic failure from those who have isolated or pure autonomic failure (idiopathic orthostatic hypotension). Biochemical and pharmacological assessments of autonomic function also differentiate multiple system atrophy from idiopathic orthostatic hypotension. In both multiple system atrophy and idiopathic orthostatic hypotension, plasma norepinephrine levels fail to increase upon standing; however, the supine norepinephrine level is low only in patients with idiopathic orthostatic hypotension.2 In multiple system atrophy, an otherwise intact peripheral sympathetic nervous system appears not to be appropriately activated whereas in idiopathic orthostatic hypotension this portion of the nervous system seems to be directly involved. This distinction is further supported by investigations of pressor sensitivity3 and neuronal uptake of norepinephrine.4 Diminished or absent epinephrine"6 and pancreatic polypeptide7 responses to insulin-induced hypoglycaemia indicate that the pandysautonomia Address for reprint requests: