Psychosomatic Medicine Faster Service from Outside North America
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Cameron, O. G.
Right arrow Articles by Curtis, G. C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cameron, O. G.
Right arrow Articles by Curtis, G. C.

Psychosomatic Medicine, Vol 58, Issue 4 289-301, Copyright © 1996 by American Psychosomatic Society

ORIGINAL ARTICLES

Platelet alpha 2-adrenoreceptors, catecholamines, hemodynamic variables, and anxiety in panic patients and their asymptomatic relatives

OG Cameron, CB Smith, RM Nesse, EM Hill, PJ Hollingsworth, JA Abelson, M Hariharan and GC Curtis
Department of Psychiatry, University of Michigan Medical Center, Ann Arbor 48109-0722, USA.

The objectives of this study were to a) replicate our prior finding of a decreased number (Bmax) of platelet alpha 2-adrenoreceptors in panic disorder, b) determine if binding is also decreased in asymptomatic first-degree relatives of panic patients (known to be at increased risk for developing panic), and c) evaluate the effect of treatment on the presumptive decrease in binding (i.e., is the decrease a state or a trait marker for panic?). Panic patients had clonidine and yohimbine platelet-binding assays, symptom ratings, and measurement of lying and standing plasma epinephrine, norepinephrine, systolic and diastolic blood pressure, and heart rate before treatment, after approximately 2 months of medication (fluoxetine, tricyclics, or alprazolam) and/or cognitive behavioral treatment, and after symptom remission while drug free; normal subjects had determinations of the same measures at approximately the same time intervals. Relatives of both groups had one determination only of all measures. Tritiated clonidine binding was decreased and lying heart rate was increased in patients before treatment. Magnitude of binding decrease was correlated with symptom severity and standing norepinephrine. No binding abnormality was seen in first-degree relatives of patients. Treatment increased clonidine binding in patients. Both patients and relatives of patients showed significantly increased standing plasma norepinephrine in comparison to controls. There is a state-related decrease in binding, associated with symptom severity and norepinephrine, in panic disorder. Abnormal reactivity of norepinephrine to standing might be a marker for increased likelihood of panic development in individuals at risk.


This article has been cited by other articles:


Home page
 Arch Gen PsychiatryHome page
O. G. Cameron, G. C. Huang, T. Nichols, R. A. Koeppe, S. Minoshima, D. Rose, and K. A. Frey
Reduced {gamma}-Aminobutyric AcidA-Benzodiazepine Binding Sites in Insular Cortex of Individuals With Panic Disorder
Arch Gen Psychiatry, July 1, 2007; 64(7): 793 - 800.
[Abstract] [Full Text] [PDF]

Home page
 Psychosom. Med.Home page
O. G. Cameron, J. K. Zubieta, L. Grunhaus, and S. Minoshima
Effects of Yohimbine on Cerebral Blood Flow, Symptoms, and Physiological Functions in Humans
Psychosom Med, July 1, 2000; 62(4): 549 - 559.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1996 by the American Psychosomatic Society