Effects of intravenously infused pituitary adenylate cyclase-activating polypeptide on adenohypophyseal Hormone secretion in normal men

• Published in: Neuroendocrinology Vol. 64; no. 3; p. 242
• Main Authors: Chiodera, P, Volpi, R, Capretti, L, Caffarri, G, Magotti, M G, Coiro, V
• Format: Journal Article
• Language: English
• Published: Switzerland S. Karger AG 01.09.1996
• Subjects: Adult; Humans; Infusions, Intravenous; Male; Neuropeptides - pharmacology; Pituitary Adenylate Cyclase-Activating Polypeptide; Pituitary Hormones, Anterior - secretion; Reference Values; Secretory Rate - drug effects; Vasoactive Intestinal Peptide - pharmacology
• ISSN: 0028-3835; 1423-0194
• DOI: 10.1159/000127124

The possible stimulatory effects of an intravenous infusion of increasing amounts of pituitary adenylate cyclase-activating polypeptide (PACAP) on anterior pituitary hormone secretions were evaluated in humans. Successively increasing doses of PACAP-38 (2, 4 and 8 pmol.kg-1.min-1; each dose for 20 min) were infused i.v. in 7 normal male subjects. On a different occasion, the same subjects were tested with vasoactive intestinal peptide (VIP; 4 pmol.kg-1.min-1 for 60 min). Circulating GH, ACTH, PRL, TSH and gonadotropin concentrations were measured before PACAP infusion and every 20 min, just before increasing the infusion dose of PACAP. Blood samples were taken before and every 15 min after the beginning of VIP administration. Serum levels of GH, TSH and gonadotropins did not change during PACAP or VIP infusion. Circulating ACTH and PRL concentrations were not modified by the infusion of the lowest dose of PACAP, whereas they were significantly increased in a dose-response fashion when higher amounts of PACAP were given. PRL, but not ACTH levels were significantly increased by VIP infusion. These data show for the first time in humans that ACTH and PRL secretions from the anterior pituitary gland are stimulated by the systemic administration of PACAP. In addition, since VIP stimulated only PRL secretion, PACAP-induced ACTH release appears to be mediated by specific receptors.