February 1989

Altered Central α2-Adrenoceptor Sensitivity in Panic Disorder

Author Affiliations

From the University Department of Psychiatry, Warneford Hospital, Oxford, England. Dr Nutt is now with the Reckitt and Colman Psychopharmacology Unit, The Medical School, University Walk, Bristol, United Kingdom.

Arch Gen Psychiatry. 1989;46(2):165-169. doi:10.1001/archpsyc.1989.01810020067011

• The possibility that a disorder of brain α2-adrenoceptor sensitivity might contribute to the etiology of panic disorder was examined using a challenge paradigm with the α2-adrenoceptor agonist clonidine. The cardiovascular, psychological, and endocrine actions of 1.5-μg/kg clonidine hydrochloride given intravenously were assessed in 16 patients and compared with age- and sex-matched controls. Patients with panic disorder showed an increased fall in blood pressure and decreased sedative and endocrine responses as compared with controls. These results suggest that there may be subsensitivity of some, and supersensitivity of other, brain α2-adrenoceptors in panic disorder. In view of the increased cardiovascular responses seen in the present study and other reports of increased responses to the α2-adrenoceptor antagonist yohimbine, there may exist an increased lability (decreased damping) of cardiovascular control mechanisms in panic disorder. Such a dysfunction could contribute to the symptoms of panic attacks, such as dizziness, palpitations, and faintness.