L. Foppiani et al., LACK OF EFFECT OF DESMOPRESSIN ON ACTH AND CORTISOL RESPONSES TO OVINE CORTICOTROPIN-RELEASING HORMONE IN ANOREXIA-NERVOSA, European journal of clinical investigation, 26(10), 1996, pp. 879-883
Citations number
25
Categorie Soggetti
Medicine, Research & Experimental","Medicine, General & Internal
Both arginine vasopressin (AVP) and corticotropin-releasing hormone (C
RH) are involved in the release of ACTH in man. Desmopressin (DDAVP),
a synthetic analogue of AVP, has been shown to have a CRH-like action
(able to promote ACTH and cortisol release) in animals but not in norm
al man. Nevertheless, DDAVP is able to release ACTH and cortisol in AC
TH-dependent Gushing's disease. We studied eight anorexia nervosa (AN)
patients [as AN is a condition in which chronic activation of the hyp
othalamic-pituitary-adrenal (HPA) axis is commonly reported] in a refe
eding phase of the disease, to evaluate whether, after weight gain, AC
TH and cortisol response to ovine corticotropin-releasing hormone (oCR
H) [1 mu g kg(-1) body weight (BW) i.v.] is restored. We also wanted t
o ascertain the effect on the HPA axis of 10 mu g i.v. DDAVP alone and
as pretreatment to oCRH (1 mu g kg(-1) BW i.v.)-induced secretion of
ACTH and cortisol. We studied six normal women as control subjects. No
significant differences in ACTH and cortisol responses to oCRH were f
ound between AN patients and control subjects. DDAVP was not able to s
timulate ACTH or cortisol release in AN patients or in control subject
s, but in the latter it was able to significantly enhance (P<0.05) ACT
H [area under curve (AUG): 590.0 +/- 104.4 pmol L(-1) 120 min(-1)] and
cortisol (AUC: 28899.0 +/- 6935.2 nmol L(-1) 120 min(-1)) responses t
o oCRH (ACTH AUC: 325.7 +/- 101.7 pmol L(-1) 120 min(-1), cortisol AUC
: 14197.4 +/- 2930.0 nmol L(-1) 120 min(-1)). The present data show th
at DDAVP does not stimulate ACTH and cortisol in AN patients or, as pr
eviously reported, in normal subjects. However, DDAVP is able to enhan
ce ACTH and cortisol release after administration in normal subjects b
ut not patients. This finding could be due to a down-regulation of hyp
ophyseal DDAVP V3 receptors in AN as a direct consequence of the hyper
cortisolaemic status usually present.