Vasopressin Effect on Cortisol Incretion in Man

Abstract

The release of ACTH is triggered by a variety of polypeptidic substances (corticotropin-releasing factors or CRF’s), elaborated at the level of the hypothalamic median eminence and delivered into pituitary portal vessel blood (1, 2, 3, 4). Between the substances exhibiting CRF-like activity, beta-CRF, alpha1-CRF and alpha2-CRF are not chemically defined (1, 4, 5), whereas the structure of vasopressin and other synthetic analogues, also exhibiting CRF-like activity is established (2). The vasopressin triggers ACTH release in normal (2), corticosteroid-pretreated (2, 6, 7) and, at variable degree, morphine or morphine-pentobarbital (6, 7, 9, 10, 11) pretreated animals. In man the studies with vasopressin are scanty. The lysine vasopressin enhances ACTH (8) and Cortisol (12, 13, 14) plasma levels in normal subjects; adrenal response is inhibited by morphine pretreatment (14, 15). Conflicting results have been reported in corticosteroid—pretreated subjects (failure (14) or raised threshold (13) for the response of ACTH release); to define the problem we have studied the effects of i.v. vasopressin on plasma Cortisol levels after dexa-methasone pretreatment in man.