Noradrenergic neuronal dysregulation in panic disorder: the effects of intravenous yohimbine and clonidine in panic disorder patients

Authors

  • D. S. Charney,

    Corresponding author
    1. Psychiatry Service, West Haven Veterans Administration Medical Center, West Haven
    2. Department of Psychiatry, Yale University School of Medicine, New Haven
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  • S. W. Woods,

    1. Department of Psychiatry, Yale University School of Medicine, New Haven
    2. Ribicoff Research Facilities, Connecticut Mental Health Center, New Haven, Connecticut, USA
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  • J. H. Krystal,

    1. Psychiatry Service, West Haven Veterans Administration Medical Center, West Haven
    2. Department of Psychiatry, Yale University School of Medicine, New Haven
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  • L. M. Nagy,

    1. Psychiatry Service, West Haven Veterans Administration Medical Center, West Haven
    2. Department of Psychiatry, Yale University School of Medicine, New Haven
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  • G. R. Heninger

    1. Department of Psychiatry, Yale University School of Medicine, New Haven
    2. Ribicoff Research Facilities, Connecticut Mental Health Center, New Haven, Connecticut, USA
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D. S. Charney, Psychiatry Service, West Haven Veterans Administration Medical Center, 950 Campbell Avenue, West Haven, CT 06516, USA

Abstract

In order to evaluate possible abnormal noradrenergic neuronal functional regulation in patients with panic disorder, the behavioral, biochemical and cardiovascular effects of intravenous yohimbine (0.4 mg/kg) and clonidine (2 μg/kg) were determined in 15 healthy subjects and 38 patients with panic disorder. A subgroup of 24 panic disorder patients were observed to experience yohimbine-induced panic attacks and had larger yohimbine-induced increases in plasma 3-methoxy-4-hydroxyphenylglycol (MHPG) than healthy subjects and other panic disorder patients. A blunted growth hormone response to clonidine and a significant clonidine-induced decrease in plasma MHPG was also observed in this subgroup of panic disorder patients. These data replicate and extend previous investigations, which are consistent with a large body of preclinical and human data relating increased noradrenergic neuronal function to human anxiety and fear states.

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