Astressin B, a corticotropin-releasing hormone receptor antagonist, accelerates the return to normal luteal function after an inflammatory-like stress challenge in the rhesus monkey.

Détails

ID Serval
serval:BIB_7444A63E5CF2
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Astressin B, a corticotropin-releasing hormone receptor antagonist, accelerates the return to normal luteal function after an inflammatory-like stress challenge in the rhesus monkey.
Périodique
Endocrinology
Auteur(s)
Xiao E., Xia-Zhang L., Vulliemoz N., Rivier J., Ferin M.
ISSN
0013-7227 (Print)
ISSN-L
0013-7227
Statut éditorial
Publié
Date de publication
02/2007
Peer-reviewed
Oui
Volume
148
Numéro
2
Pages
841-848
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, N.I.H., Extramural
Publication Status: ppublish
Résumé
Endogenous release of CRH in stress has been associated with a dysfunctional reproductive endocrine axis. In the rhesus monkey, an inflammatory-like stress challenge in the luteal phase decreases luteal secretory function. Here, we tested the effectiveness of astressin B, a nonspecific CRH receptor antagonist, in constraining the deleterious impact of a 10-d lipopolysaccharide (LPS) challenge on the menstrual cycle. Two protocols were carried out in nine animals. In the first, the animals, after showing two normal consecutive control cycles, were injected daily for 10 days with LPS (75-125 mug/d) during the luteal phase of the cycle. The animals were followed through the two postchallenge cycles. The second protocol, carried out in the following year, was identical with protocol 1, except that the animals were treated with astressin B (0.45 mg/kg) 1 h before each daily LPS challenge during the luteal phase. Blood samples were obtained daily to document cyclic hormones levels. The LPS challenge significantly decreased luteal progesterone and LH release during the challenge cycle. Inhibition of luteal progesterone extended to the two successive postchallenge cycles. Astressin B treatment prevented luteal LH but not luteal progesterone decrease during the treatment cycle and restored normal progesterone secretion during the two posttreatment cycles. We conclude that the deleterious impact of a short-term inflammatory stress challenge on luteal function is far longer than the stress period itself. Systemic administration of astressin B accelerates the return to normal luteal function, presumably by restoring normal neuroendocrine regulation of gonadotropin secretion.
Mots-clé
Animals, Corpus Luteum/drug effects, Corpus Luteum/metabolism, Corticotropin-Releasing Hormone/pharmacology, Eating/drug effects, Female, Gonadotropins/metabolism, Hydrocortisone/metabolism, Inflammation/chemically induced, Inflammation/metabolism, Injections, Intravenous, Lipopolysaccharides/administration & dosage, Lipopolysaccharides/antagonists & inhibitors, Lipopolysaccharides/pharmacology, Luteal Phase, Macaca mulatta, Menstrual Cycle/drug effects, Peptide Fragments/pharmacology, Receptors, Corticotropin-Releasing Hormone/antagonists & inhibitors, Recovery of Function, Stress, Physiological/chemically induced, Stress, Physiological/metabolism, Time Factors
Pubmed
Web of science
Open Access
Oui
Création de la notice
02/10/2019 19:39
Dernière modification de la notice
07/10/2019 5:26
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