• 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