Chronic Treatment with an Agonist of Gonadotropin-Releasing Hormone Enhances Luteal Function in Cattle

• Published in: Biology of reproduction 2003-08, Vol.69 (2), p.398-403
• Main Authors: T.L. Davis, M.L. Mussard, H. Jimenez-Severiano, W.J. Enright, J.E. Kinder
• Format: Article
• Language: English
• Subjects: Animals; Behavior, Animal - drug effects; Biological and medical sciences; Cattle; Corpus Luteum - anatomy & histology; Corpus Luteum - diagnostic imaging; Corpus Luteum - drug effects; Corpus Luteum Maintenance - drug effects; Estrous Cycle - physiology; Female; Fundamental and applied biological sciences. Psychology; Gonadotropin-Releasing Hormone - agonists; Hormone metabolism and regulation; Luteinizing Hormone - blood; Mammalian female genital system; Nafarelin - analogs & derivatives; Nafarelin - pharmacology; Ovulation - drug effects; Pregnancy; Progesterone - blood; Radioimmunoassay; Ultrasonography; Vertebrates: reproduction
• ISSN: 0006-3363; 1529-7268
• DOI: 10.1095/biolreprod.102.013821

Our hypothesis was that luteal function, as determined by plasma progesterone concentrations, and corpus luteum (CL) size is enhanced in cattle administered an agonist of GnRH when the CL is developing as compared with administration of an agonist when the CL is fully functional. Cattle were chronically administered a GnRH agonist, azagly-nafarelin, from Day 3 to Day 21 (D3) or Day 12 to Day 21 (D12) or served as untreated control females (Day 0 = behavioral estrus). Blood samples were serially collected on Days 7 and 14 to evaluate LH secretory patterns and twice daily to measure plasma progesterone. Ultrasonographic examinations were conducted daily to record the area of the CL. CL size and plasma progesterone concentrations were both enhanced in the D3 group as compared with the control group. Progesterone was increased in the D12 group on Days 16 and 17 as compared with the control females. Treatment with GnRH agonist increased basal and mean LH concentrations in both D3 and D12 groups as compared with the controls. We rejected our hypothesis because chronic administration of a GnRH agonist increased plasma progesterone when administered both when the CL was developing and when it was fully functional. The enhanced luteal function was likely due to increased basal LH.