Sex hormones and the motility of and prostaglandin output from, uterine horns of immature rats.

The effects of injecting estradiol, progesterone or both hormones to immature rats, on the spontaneous contractions of isolated uterine horns and on prostaglandin (PG) E and F-like materials released into the bathing medium, were studied. The in vitro contractile decrement detected both in controls as well as in the group receiving progesterone (P4) alone, was only minor. On the other hand, preparations from rats treated with 17-beta-estradiol (E2) exhibited a significant and progressive reduction of spontaneous motility. Coincident with these smaller contractions a significant diminution of PGE-output accompanied by an enhancement of the release of PGF-like material into the suspending solution, were found. The initial (postisolation) isometric developed tension (IDT) of uterine preparations from immature rats injected with sex hormones was significantly higher than that of tissues from untreated control animals. Neither the initial contractile frequency (CF) nor its constancy changed following hormonal treatment (E2 or P4), except in the case of uteri from animals treatment (E2 or P4), except in the case of uteri from animals administered with P4, which showed a smaller decrement of CF than controls. Furthermore, tissue preparations obtained from animals injected with P4 released into the bathing media similar amounts of PGE-like material as controls, but significantly more PGF. It is interesting that the injection of E2 plus P4 increased the output of PGE-like material but did not modify that of PGE i. e., the depressive effect of estradiol on the release of PGE into the bathing media was abolished by the administration of P4. On the other hand, the addition of indomethacin or acetylsalicylic acid to the bath solution reduced significantly contractions of uterine horns isolated from immature animals. The foregoing results, supporting our previous findings on the effect of P4 on PGF release from the rat uterus, are in keeping with the hypothesis holding that better spontaneous motility correlates well with a greater release of PGE and that E2 injection coincides with a depression of both PGE output and myometrial contractions.