title: Physiological roles of prolactin in the adrenocortical response to acute restraint stress.
abstract: The present study characterized the different hormonal responses to stress in the endocrine milieu with different circulating levels of prolactin (PRL) and examined the direct effects of PRL on adrenal steroidogenic responses to adrenocorticotropic hormone (ACTH) using experimentally induced hyperprolactinemia and hypoprolactinemia male rat models. Hyperprolactinemia was induced by transplantation of two adult female rat anterior pituitary glands under the kidney capsule for 2 weeks, and hypoprolactinemia was induced by daily subcutaneous injection of 2-Bromo-alpha-Ergocryptine (CB-154) for 2 weeks. Under stress conditions, the peak levels of ACTH were significantly higher in hypoprolactinemia than normal rats. Meanwhile, the peak levels of corticosterone and progesterone were significantly higher in hyperprolactinemia than in normal and hypoprolactinemia stressed rats. Results of in vitro experiments showed that adrenocortical cells in hyperprolactinemia exhibited higher basal levels of corticosterone and progesterone rats than normal and hypoprolactinemia rats. The stimulatory effect of ACTH on corticosterone and progesterone release was higher in hyperprolactinemia than hypoprolactinemia rats. In addition, PRL increased the stimulatory effect of ACTH-induced corticosterone secretion in all rat models. These results suggest that hypoprolactinemia and hyperprolactinemia rats exhibit marked differences in the response of their hypothalamic-pituitary-adrenal (HPA) axis during acute restrain stress. Additionally, these studies emphasize that the adrenal cortex might be more sensitive to ACTH stimulation in endocrine milieu with high levels of PRL resulting in high corticosterone and progesterone release.
authors.affiliation: Department of Basic Veterinary Science, The United School of Veterinary Sciences, Gifu University, Japan.
authors.forename: Sukanya
authors.initials: S
authors.lastname: Jaroenporn
authors.forename: Kentaro
authors.initials: K
authors.lastname: Nagaoka
authors.forename: Chizuru
authors.initials: C
authors.lastname: Kasahara
authors.forename: Ryo
authors.initials: R
authors.lastname: Ohta
authors.forename: Gen
authors.initials: G
authors.lastname: Watanabe
authors.forename: Kazuyoshi
authors.initials: K
authors.lastname: Taya
mesh_terms: D000302:Adrenal Cortex / Q000187:drug effects / Q000378:metabolism*; D000324:Adrenocorticotropic Hormone / Q000494:pharmacology; D000818:Animals; D003345:Corticosterone / Q000378:metabolism; D005260:Female; D006966:Hyperprolactinemia / Q000378:metabolism; D007030:Hypothalamo-Hypophyseal System / Q000187:drug effects / Q000378:metabolism; D008297:Male; D010913:Pituitary-Adrenal System / Q000187:drug effects / Q000378:metabolism; D011374:Progesterone / Q000378:metabolism; D011388:Prolactin / Q000097:blood / Q000494:pharmacology / Q000502:physiology*; D051381:Rats; D017208:Rats, Wistar; D012149:Restraint, Physical / Q000502:physiology*; D013315:Stress, Psychological / Q000378:metabolism*