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The Effect of Mianserin on Alpha-2 Adrenergic Receptor Function in Depressed Patients

Published online by Cambridge University Press:  29 January 2018

Dennis S. Charney
Affiliation:
Department of Psychiatry, Connecticut Mental Health Center, Yale University School of Medicine, 34 Park Street, New Haven, CT 06508, USA
George R. Heninger
Affiliation:
Department of Psychiatry, Connecticut Mental Health Center, Yale University School of Medicine, 34 Park Street, New Haven, CT 06508, USA
David E. Sternberg
Affiliation:
Falkirk Hospital, Central Valley, NY 10917, USA

Summary

Recent clinical investigations have shown that long term treatment with the tricyclic antidepressants desipramine and amitriptyline reduces the sensitivity of the alpha-2 adrenergic autoreceptor. In order to determine whether the tetracyclic antidepressant mianserin also has this action, the effect of clonidine, an alpha-2 adrenergic receptor agonist, on plasma levels of the norepinephrine metabolite 3-methoxy-4-hydroxyphenlethyleneglycol (MHPG), blood pressure, and patient-rated sedation were measured in fifteen depressed patients before and during mianserin treatment. Postsynaptic alpha-2 adrenergic receptor function was assessed by measuring the growth hormone response to clonidine before and during treatment. Mianserin had little or no effect on the ability of clonidine to lower plasma MHPG and blood pressure, and to increase sedation and growth hormone secretion. The findings of this investigation indicates that long term mianserin treatment does not produce significant subsensitivity of the alpha-2 adrenergic receptor and suggests that a reduction in alpha-2 adrenergic autoreceptor sensitivity is not a necessary action for all effective antidepressant treatments.

Type
Papers
Copyright
Copyright © 1984 The Royal College of Psychiatrists 

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