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Relationship between endometrial oxytocin receptors and oxytocin-induced prostaglandin F₂ release during the oestrous cycle and early pregnancy in pony mares

The effect of transcervical endometrial biopsy on the concentrations of plasma immunoreactive oxytocin and 15-keto-13,14-dihydro-prostaglandin F₂ (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. Five biopsy specimens were taken within 15 min and consecutive specimens from each mare were pooled two (A) and three (B) together for measurement of the number of oxytocin receptors. Blood samples were collected at intervals of 5 min for 15 min beginning just before the initial biopsy. Biopsy procedure elicited prompt oxytocin release in all mares. Pregnancy did not affect the response but day after ovulation had a significant influence on oxytocin release. The greatest increase in plasma oxytocin was observed on day 12 in both nonpregnant and pregnant mares and the lowest on day 8. The concentration of plasma PGFM rose linearly over the 15 min period in nonpregnant mares. This response increased progressively with time after ovulation and was greatest on day 14. There was no increase in circulating PGFM in pregnant mares. Endometrial oxytocin receptor concentration was lowest in mares at oestrus and 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 receptors was lower in pregnant than in nonpregnant mares. Because of the positive correlation between PGF₂ release, endometrial oxytocin receptor density, and plasma oxytocin concentrations in non-pregnant mares, it is assumed that the release of PGF₂ was induced by oxytocin and was mediated by oxytocin receptors. Pregnancy-induced inhibition of PGF₂ release was not associated with suppression of oxytocin release or oxytocin receptor density. An embryoderived factor is therefore the most likely cause for the suppression of PGF₂ release and interruption of the oxytocin–PGF₂ interaction in mares during early pregnancy.

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