Effect of Progesterone and Estradiol-17β on Oxytocin-Induced PGF2α Release and Endometrial Oxytocin Receptor Concentrations in Ovariectomized Goats

1998 
The effects of progesterone and estradiol-17β on oxytocin-induced prostaglandin (PG)F2α release and on endometrial oxytocin receptor concentrations were examined in ovariectomized goats. Each goat received a progesterone + estradiol-17β pretreatment schedule for 6 days aimed at mimicking steroid hormone changes prior to estrus, and inducing both a preovulatory-like LH surge and estrous behaviour. Goats were then assigned to treatment groups, i.e., 1) control, 2) progesterone, 3) estradiol-17β, and 4) progesterone + estradiol-17β. In each group, (n = 4) on Days 3, 6, 9, 12, and 15 of the 15 day treatment period, each goat received 10 i.u. oxytocin i.v. Jugular blood samples were taken to monitor any changes in concentrations of 13, 14 dihydro-15-keto prostaglandin F2α (PGFM). No changes in PGFM were observed in any group in response to oxytocin on Days 3, 6, and 9. On Day 12, however, there was a significant response in the progesterone + estradiol-17β-treated goats (Group 4) and on Day 15, larger responses were observed in both Group 2 (progesterone-alone) and Group 4. Both peak response (p < 0.05) and the area under the concentration vs. time curve (p < 0.001) for PGFM were greater in the latter group. In a separate experiment, but using the same goats and steroid treatments, endometrial oxytocin receptor concentrations were assessed on Day 15. Receptors were observed in all four groups. While progesterone (Group 2) raised (p < 0.05) concentrations relative to those found in controls and estradiol-treated goats, combined treatment with progesterone and estradiol (Group 4) produced a further increase (p < 0.05). The results suggest that in the goat progesterone is capable of increasing oxytocin-induced PGF2α release by inducing endometrial oxytocin receptor formation. Estradiol-17β, while itself ineffective, appears to have a synergistic role in potentiating the effect of progesterone, producing an earlier and higher PGFM response to oxytocin.
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