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The superovulation of red deer hinds with eCG is commonly associated with premature luteal regression. This study was an investigation of the endocrine mechanisms regulating luteal function after superovulation. Four groups of hinds (n = 7–8 per group) were treated with progesterone-impregnated intravaginal controlled internal drug-releasing (CIDR) devices for 12 days to synchronize estrus (CIDR device withdrawal = Day 0). Group 1 served as controls; group 2 received an i.m. injection of 0.25 mg estradiol benzoate (EDB) at 72, 84, 96, and 108 h after removal of the device; group 3 received an i.m. injection of 1200 IU eCG at ‒72 h; group 4 received both EDB and eCG treatments. Oxytocin-induced prostaglandin F2α(PGF2α) release was assessed on Day 4 by oxytocin challenge. Ovarian response was determined by laparoscopy on Day 14. Plasma steroid profiles were determined from thrice-weekly plasma samples collected from Day -13 to Day 35 (progesterone) and Days 0 to 14 (estradiol). EDB increased the incidence of premature luteal regression in monovulatory and eCG-treated animals (p< 0.05) and reduced the number of CL (p< 0.05) in eCG-treated animals. EDB and eCG each elevated plasma concentrations of estradiol and increased the incidence of significant oxytocin-induced PGF2αrelease. These results support the hypothesis that eCG causes premature luteal regression by inducing prolonged estrogen secretion that sensitizes the endometrium to oxytocin, thereby eliciting PGF2αrelease during the early luteal phase.