Recent studies suggest that the α-2 noradrenergic receptor may be of pathophysiologic importance in depression and possibly eating disorders. To assess this further, we administered 1.3 μ/kg i.v. clonidine to 14 bulimics and 11 controls and measured in blood GH, cortisol, MHPG, VMA, HVA, and cardiovascular responses pre- and postperturbation. There were no significant differences between groups in cardiovascular or endocrine responses except for HVA, where baseline levels were higher in controls and demonstrated a greater drop postclonidine than in bulimics. Depressed bulimics responded similarily to nondepressed bulimics. These results are different from those found in depressed patients were there are blunted growth hormone responses to clonidine and differential responses in MHPG, compared with controls, suggesting reduced responsiveness of α-2 noradrenergic receptors. With regard to noradrenergic receptor responsivity, these data do not support shared biologic abnormalities in depression and bulimia nervosa.
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Kaplan et al. (1989) studied this question.
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