Effects of exogenous oxytocin and progesterone on GnRH-induced short luteal phases in anoestrous ewes.
Two experiments investigate the effects of oxytocin and progesterone on premature luteolysis in ewes. In Expt 1, 20 anoestrous ewes were induced to ovulate by multiple injections of GnRH (250 ng i.v. every 2 h for 24 h) followed by a bolus injection of GnRH (125 micrograms, i.v.). Ten ewes received a continuous infusion of oxytocin from the day after the GnRH bolus injection and the other ten ewes were infused with saline. Oxytocin infusion had no significant effect on the proportion of ewes with short luteal phases (P > 0.05). All ewes that had luteal phases of normal duration from either group (n = 9) exhibited a transient increase in plasma concentrations of progesterone 2 h after insertion of the pump. In Expt 2, 25 anoestrous ewes were treated with GnRH as in Expt 1. Five ewes were pretreated with progestagen for 11 days and ten ewes received progesterone (12 mg, i.m.) 24 h after the bolus injection of GnRH. All animals received an oxytocin injection (1 microgram, i.v.) on day 4 after the GnRH bolus. All five ewes that were pretreated with progestagen had normal luteal function and none exhibited a 13, 14-dihydro-15-keto PGF2 alpha (PGFM) response to oxytocin. None of the ten ewes injected with progesterone had a normal luteal phase and six ewes exhibited a PGFM response to oxytocin. Four ewes in the control group had normal luteal function and three had short luteal phases. It is concluded that (1) administration of oxytocin from about the time of ovulation does not prevent premature luteal regression; (2) a transient increase in progesterone at about the time of ovulation is associated with luteal phases of normal duration; (3) a more extended exposure to progesterone at about the time of ovulation prevents normal luteal function and may inhibit luteinization and (4) pretreatment with progesterone prevents luteolysis by reducing the uterine response to oxytocin early in the luteal phase.
Beard
A P
AP
Department of Physiology and Environmental Science, University of Nottingham, Leics, UK.
Hunter
M G
MG
D000780:Anestrus / Q000502:physiology*; D000818:Animals; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000494:pharmacology*; D008183:Luteal Phase / Q000187:drug effects*; D010121:Oxytocin / Q000494:pharmacology*; D011374:Progesterone / Q000097:blood / Q000494:pharmacology*; D018045:Receptors, Oxytocin / Q000378:metabolism; D012756:Sheep / Q000097:blood* / Q000378:metabolism; D014599:Uterus / Q000187:drug effects
D018045:Receptors, Oxytocin; C008228:15-keto-13,14-dihydroprostaglandin F2alpha; D007987:Gonadotropin-Releasing Hormone; D011374:Progesterone; D010121:Oxytocin; D015237:Dinoprost