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Abstract
Benzodiazepine receptors appear to mediate both the anxiolytic effects of benzodiazepine drugs and the anxiogenic effects of several benzodiazepine inverse agonists (Tallman and Gallagher 1985). Evidence that brain benzodiazepine receptor density is decreased in genetically fearful strains of rats (Robertson et al. 1978) suggests that human anxiety states might be associated with decreased functioning of the benzodiazepine system. This hypothesis has not been tested in humans. Recently, using a tritiated norepinephrine (NE) isotope dilution technique, we showed that a single oral dose of 15 mg of diazepam suppresses sympathetic nervous system (SNS) outflow as reflected by a fall in plasma NE appearance rate (NEA) and plasma epinephrine (EPI) (Roy-Byrne et al. 1988). This suggests that central nervous system (CNS) benzodiazepine pathways play a role in the regulation of
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