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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

Department of Obstetrics and Gynecology (E.X., L.X.-Z., N.V., M.F.), College of Physicians and Surgeons, Columbia University, New York, New York 10032; and The Salk Institute (J.R.), La Jolla, California 92186

Address all correspondence and requests for reprints to: Michel Ferin, Department of Obstetrics and Gynecology, Columbia University, College of Physicians and Surgeons, 630 West 168th Street, New York, New York 10032. E-mail: mf8{at}columbia.edu.

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 µg/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.

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