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Vol. 47, No. 2, 2003
Issue release date: April 2003
Section title: Biological Psychology/Pharmacopsychology. Editor: P. Netter (Giessen). Original Paper
Neuropsychobiology 2003;47:102–108
(DOI:10.1159/000070018)

Endocrine and Cardiovascular Responses to Corticotropin-Releasing Hormone in Patients with Posttraumatic Stress Disorder: A Role for Atrial Natriuretic Peptide?

Kellner M. · Yassouridis A. · Hübner R. · Baker D.G. · Wiedemann K.
aDepartment of Psychiatry and Psychotherapy, University Hospital Hamburg-Eppendorf, Hamburg, bMax Planck Institute of Psychiatry, Clinical Institute, Munich, Germany; cDepartment of Psychiatry, University of Cincinnati and Cincinnati VA Medical Center, Cincinnati, Ohio, USA

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Article / Publication Details

First-Page Preview
Abstract of Biological Psychology/Pharmacopsychology. Editor: P. Netter (Giessen). Original Paper

Published online: 4/25/2003

Number of Print Pages: 7
Number of Figures: 0
Number of Tables: 2

ISSN: 0302-282X (Print)
eISSN: 1423-0224 (Online)

For additional information: http://www.karger.com/NPS

Abstract

Hypothalamic-pituitary-adrenocortical (HPA) axis data, such as low plasma cortisol concentrations in spite of increased corticotropin-releasing hormone (CRH) levels in patients with posttraumatic stress disorder (PTSD), are difficult to interpret. Atrial natriuretic peptide (ANP) may be an explanatory link in the neuroendocrine pathophysiology of the disorder, since it is a neuromodulator with antianxiety effects that inhibits HPA activity at multiple levels. Seventeen patients with chronic PTSD and 17 healthy control subjects were given 100 µg of human CRH at 3 p.m. ANP, adrenocorticotropic hormone (ACTH), and cortisol levels in plasma as well as blood pressure and heart rate were measured during basal conditions and after CRH stimulation. Basal ANP levels were significantly lower in PTSD patients in comparison with normal controls, but the response to CRH was undistinguishable. In contrast to our expectation, no significant differences in basal or CRH-stimulated ACTH or cortisol parameters could be observed. Systolic and diastolic blood pressures at baseline and after CRH were significantly elevated in PTSD patients. All group differences remained significant after controlling for basal blood pressure and/or body mass index. Our data do not support a role of ANP in abnormal HPA axis regulation in PTSD. However, the persistently low ANP plasma levels in PTSD patients despite elevated blood pressure may serve to facilitate anxiety behavior and have adverse long-term cardiovascular consequences. Further studies to assess ANP secretion in PTSD patients and to clarify its pathophysiological impact are needed.


  

Author Contacts

PD Dr. Michael Kellner
Department of Psychiatry and Psychotherapy
University Hospital Hamburg-Eppendorf, Martinistrasse 52
D–20246 Hamburg (Germany)
Tel. +49 40 42803 3223, Fax +49 40 42803 3461, E-Mail kellner@uke.uni-hamburg.de

  

Article Information

Number of Print Pages : 7
Number of Figures : 0, Number of Tables : 2, Number of References : 55

  

Publication Details

Neuropsychobiology
Founded 1975 by J. Mendlewicz (Brussels)
Official Journal of the International Pharmaco-EEG Society (IPEG)

Vol. 47, No. 2, Year 2003 (Cover Date: Released April 2003)

Journal Editor: P. Netter, Giessen; J. Mendlewicz, Brussels; B. Saletu, Vienna
ISSN: 0302–282X (print), 1423–0224 (Online)

For additional information: http://www.karger.com/nps


Article / Publication Details

First-Page Preview
Abstract of Biological Psychology/Pharmacopsychology. Editor: P. Netter (Giessen). Original Paper

Published online: 4/25/2003

Number of Print Pages: 7
Number of Figures: 0
Number of Tables: 2

ISSN: 0302-282X (Print)
eISSN: 1423-0224 (Online)

For additional information: http://www.karger.com/NPS


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