Gap Junction Modulation in Rat Uterus. II. Effects of Antiestrogens on Myometrial and Serosal Cells 1

Publisher Website
Google Scholar
Abstract
The ability of several triphenylethylene antiestrogens to affect the modulation of gap junctions in rat uterine myometrial and serosal cells was examined in animals 60 days following hypophysectomy. Five daily injections of enclomiphene, zuclomiphene, tamoxifen, nafoxidine, CI-628 [1-{2-[p-[.alpha.-(p-methoxyphenyl)-.beta.-nitro-styryl]phenoxy]ethyl}pyrrolidine monocitrate] or CI-680 [3-[p-[.alpha.-(p-methoxyphenyl)-.beta.-nitrostyryl]phenoxy]-N,N-dimethylpropylamine monocitrate] (500 .mu.g per injection) promote uterine luminal epithelial cell hypertrophy characteristic of exogenous estrogen administration. These same compounds, however, fail to induce myometrial cell or increase the number of serosal cell gap junctions, respectively, which is also characteristic of exogenous estrogen treatment. Pretreatment of animals with antiestrogens blocks the ability of estradiol benzoate (E2 B) to induce gap junction formation in myometrial cells when followed by combined injections of E2 B and antiestrogens (both 250 .mu.g) administered daily for 5 days. Therefore, with respect to the parameter of myometrial cell gap junction stimulation, all of the antiestrogens examined act as pure estrogen antagonists. These same antiestrogen pretreatments only weakly antagonized the ability of E2 B to modulate serosal cell gap junction membrane. Different mechanisms may exist for the estrogenic modulation of gap junctional membrane in myometrial and serosal cells.

This publication has 2 references indexed in Scilit: