Influence of cholinergic receptor blockade on drug-induced prolactin release in the monkey

• Published in: Hormone research Vol. 7; no. 2; p. 118
• Main Authors: Gala, R R, Subramanian, M G, Peters, J A, Jaques, Jr, S
• Format: Journal Article
• Language: English
• Published: Switzerland 01.01.1976
• Subjects: Animals; Atropine - pharmacology; Female; Haplorhini; Macaca; Perphenazine - pharmacology; Prolactin - secretion; Receptors, Cholinergic - drug effects; Serotonin - pharmacology; Thyrotropin-Releasing Hormone - pharmacology
• ISSN: 0301-0163
• DOI: 10.1159/000178719

The influence of varying doses of perphenazine, thyrotropin-releasing hormone (TRH) and serotonin on prolactin release was examined in two species of monkeys: rhesus (Macaca mulatta) and crab-eating (Macaca fascicularis). The intravenous administration of 0.33 mg/kg body weight of perphenazine or 1.0 mug/kg body weight of TRH gave a greater release of prolactin than higher doses of perphenazine (1.0 mg/kg) or TRH) (3.4 mug/kg), respectively. Prolactin release induced by serotonin at doses of 1, 5 and 10 mug/kg was similar. Both atropine sulfate (Atr-SO4) and atropine methyl nitrate (Atr-MN) at a similar base level potentiated the prolactin releasing action of the high dose of perphenazine suggesting that high doses of perphenazine activate a cholinergic inhibitory component present in the pituitary. Atropine sulfate had no potentiating action on the TRH-induced prolactin release, while Atr-MN appeared to prolong the response of TRH without potentiating it. Neither form of atropine had any influence on serotonin-induced prolactin release. The data indicated that the lower prolactin response to high doses of perphenazine and TRH were brought about by different mechanisms, and that the mechanism for perphenazine appeared to be mediated through a pituitary cholinergic system.