Autonomic nervous system activity is essential for maintaining circulatory and metabolic homeostasis. In order to study sympathetic nervous system function and its relationship to other neuroendocrine systems, it is necessary to measure neurotransmitter, hormonal, and peptide levels in response to various stimuli. The levels of norepinephrine, epinephrine, and dopamine and their metabolites in various body fluids reflect the activity of the neurones from which these neurotransmitters are released. Measurement of urinary catecholamine metabolites and their stereospecific labelling pattern following administration of radiolabelled isomers of norepinephrine provides a means for investigating the origin of norepinephrine metabolites. Cerebrospinal fluid levels of monoamine metabolities can be used to assess central nervous system neurotransmitter metabolism. It is necessary to consider the origin of these metabolites to make appropriate corrections for valid interpretations of the data. These strategies have been used to study patients with neurogenic orthostatic hypotension and in other clinical situations in which adrenergic function is abnormal. Insulin may play a role in causing post-prandial hypotension in patients with autonomic failure. The mechanism of insulin-induced hypotension may involve release of beta-endorphin without a concomitant elevation of norepinephrine or a direct effect of insulin on brain receptors. Glucose prevents the blood pressure drop following insulin administration in patients with autonomic failure attended by central neurological signs but not in patients with isolated autonomic failure. In normal subjects most vanillylmandelic acid is derived from 3-methoxy-4-hydroxyphenylglycol. Investigation of the effects of aging on autonomic nervous system function is in progress. A more thorough understanding of neurotransmitter metabolism in these clinical situations leads to more rational approaches to therapy.
