Title of article
Mineralocorticoid Receptor Function in Posttraumatic Stress Disorder After Pretreatment with Metyrapone
Author/Authors
Christian Otte، نويسنده , , Christoph Muhtz، نويسنده , , Sima Daneshkhah، نويسنده , , Alexander Yassouridis، نويسنده , , Falk Kiefer، نويسنده , , Klaus Wiedemann، نويسنده , , Michael Kellner، نويسنده ,
Issue Information
روزنامه با شماره پیاپی سال 2006
Pages
4
From page
784
To page
787
Abstract
Background
Alterations of mineralocorticoid receptor (MR) mediated negative feedback inhibition of cortisol might contribute to abnormalities of hypothalamic-pituitary adrenal (HPA) activity in posttraumatic stress disorder (PTSD).
Methods
In a placebo-controlled study, we examined 11 subjects with PTSD and 11 healthy controls between 14:00 and 21:00. After pretreatment with 3 g metyrapone to inhibit basal endogenous cortisol secretion, subjects orally received in randomized order .5 mg of the MR agonist fludrocortisone or placebo. Adrenocorticotropic hormone (ACTH), cortisol, and 11-deoxycortisol were measured every 30 min until 21:00.
Results
Compared to placebo, fludrocortisone led to a significant decrease of ACTH and cortisol that was similar in both groups. Subjects with PTSD had higher raw cortisol and higher normed (baseline-related) ACTH and 11-deoxycortisol values after metyrapone independent of treatment with fludrocortisone or placebo.
Conclusions
While HPA responses after metyrapone seem to be stronger in PTSD compared to controls, no alterations of mineralocorticoid receptor function in PTSD were found in this study.
Keywords
cortisol , posttraumatic stress disorder , mineralocorticoidreceptor , HPA axis , metyrapone
Journal title
Biological Psychiatry
Serial Year
2006
Journal title
Biological Psychiatry
Record number
503116
Link To Document