Effect of administration of corticotropin-releasing hormone and glucocorticoid on arginine vasopressinresponse to osmotic stimulus in normal subjects and patients with hypocorticotropinism without overt diabetes insipidus

Abstract

We examined the effect of CRH administrationon the response of plasma arginine vasopressin (AVP) inducedby an osmotic stimulus in six normal subjects and five patients with hypocorticotropinism without overt diabetes insipidus (four patients with Sheehan’s syndrome and one with idiopathic pituitarydwarfism with ACTH deficiency). Hypertonic salineinfusion (855 mmol/L saline solutions at a rate of 205 μmol/kgmin for 10 min) increased plasma AVP 5.7-fold (P < 0.01) innormal subjects and 2.4-fold (P <0.05) in the patients. CRHadministration significantly augmented the plasma AVP responseto the osmotic stimulus in the normal subjects, but not in the patients with hypocorticotropinism. CRH administrationalone did not influence plasma AVP. These findings suggest thata central CRH-related mechanism(s) was at least partly involved in the augmentation of AVP release. Based on the relatively lowplasma AVP response to the osmotic stimulus in patients andtheir lower plasma AVP levels and higher plasma osmolality under basal conditions, we suggest that patients with hypocorticotropinism have partial diabetes insipidus, in which impairmentof central CRH action might be, at least in part, involved.The response of plasma AVP to the osmotic stimulus wasattenuated significantly when the patients were given cortisol.Since basal PRA, plasma aldosterone, plasma osmolality, hematocrit, body weight, mean blood pressure, and heart rate weresimilar with and without cortisol administration, this effect ofcortisol may have been due to central suppression of the AVPresponse to the osmotic stimulus. © 1989 by The Endocrine Society.