RELATIONSHIP BETWEEN ENDOMETRIAL OXYTOCIN RECEPTORS AND OXYTOCIN-INDUCED PROSTAGLANDIN-F2-ALPHA RELEASE DURING THE ESTROUS-CYCLE AND EARLY-PREGNANCY IN PONY MARES

The effect of transcervical endometrial biopsy on the concentrations o f plasma immunoreactive oxytocin and 15-keto-13,14-dihydro-prostagland in F-2 alpha (PGFM) was studied in 18 pony mares on days 8, 12 and 14 after ovulation, days 12 and 14 of early pregnancy and at oestrus. Fiv e biopsy specimens were taken within 15 min and consecutive specimens from each mare were pooled two (A) and three (B) together for measurem ent of the number of oxytocin receptors. Blood samples were collected at intervals of 5 min for 15 min beginning just before the initial bio psy. Biopsy procedure elicited prompt oxytocin release in all mares. P regnancy did not affect the response but day after ovulation had a sig nificant influence on oxytocin release. The greatest increase in plasm a oxytocin was observed on day 12 in both nonpregnant and pregnant mar es and the lowest on day 8. The concentration of plasma PGFM rose line arly over the 15 min period in nonpregnant mares. This response increa sed progressively with time after ovulation and was greatest on day 14 . There was no increase in circulating PGFM in pregnant mares. Endomet rial oxytocin receptor concentration was lowest in mares at oestrus an d highest in nonpregnant mares on day 14. Oxytocin receptor density in pregnant mares was similar to that in nonpregnant mares on day 12 but was significantly attenuated on day 14. The affinity of oxytocin rece ptors was lower in pregnant than in nonpregnant mares. Because of the positive correlation between PGF(2 alpha) release, endometrial oxytoci n receptor density, and plasma oxytocin concentrations in nonpregnant mares, it is assumed that the release of PGF(2 alpha) was induced by o xytocin and was mediated by oxytocin receptors. Pregnancy-induced inhi bition of PGF(2 alpha) release was not associated with suppression of oxytocin release or oxytocin receptor density. An embryo-derived facto r is therefore the most likely cause for the suppression of PGF(2 alph a) release and interruption of the oxytocin-PGF(2 alpha) interaction i n mares during early pregnancy.