= 5) infused animals.The oxytocin infusion maintained peripheral plasma concentrations of 53 \ m=+-\ 3\ m=. \ 2pg oxytocin ml \ m=-\ 1 (mean \ m=+-\ sem) compared with values of about 1 pg ml \ m=-\ 1 during oestrus in control ewes. Oxytocin infusion had no effect on luteal phase progesterone concentrations, the timing of luteolysis, basal luteinizing hormone (LH) secretion, LH pulse frequency, or the timing or height of the LH surge. Treated ewes came into oestrus significantly earlier than controls (P < 0\m=.\05) but ovulated normally. Uterine samples collected 96 h after cloprostenol injection (approximately day 2 of the cycle) showed that oxytocin receptor concentrations were significantly higher in the endometrium in ewes that had been given a 5 day oxytocin infusion than in control animals (556 and 262fmol mg\m=-\1protein, respectively: geometric means from ANOVA, P < 0\m=.\001), whereas myometrial receptor concentrations were not affected (113 and 162 fmol mg\m=-\1 protein, respectively).We conclude that the previously reported delay in luteal development caused by oxytocin infusion is not due to the inhibition or delay of ovulation, but must instead occur via a direct influence on the developing corpus luteum. Our results differ from those in rodents in which higher doses of oxytocin have been shown to influence both LH secretion and the timing of ovulation. Prolonged infusion with oxytocin at the dose used (the high end of the normal physiological range) during the periovulatory period does not cause downregulation of the oxytocin receptor.