Oviduct contractility in non-pregnant rats: changes in estrous cycle and effects of estrogen and progesterone antagonists

Abstract

This study aimed to systematically characterize oviduct contractility across the estrous cycle and to examine the regulatory roles of estradiol and progesterone using receptor antagonists and molecular docking to explore both receptor-mediated and ion channel pathways. Female Wistar rats (n = 48) were used for this purpose. Oviducts were collected during proestrus, estrus, metestrus, and diestrus, and spontaneous contractions were recorded using an isometric force transducer. Serum levels of estradiol, progesterone, luteinizing hormone, follicle-stimulating hormone, and prolactin were measured through enzyme-linked immunosorbent assay (ELISA). To understand hormonal regulation, tamoxifen (10 mg/kg) was administered during proestrus, and mifepristone (5 mg/kg) was administered during metestrus. Immunofluorescence (IF) study was performed to evaluate expression of the estrogen, progesterone, and glucocorticoid receptors (ER, PR, and GR). Molecular docking analysis assessed interactions of the antagonists with estrogen and progesterone receptors and ion channels. Oviduct contractility was observed noticeably highest during proestrus (high estradiol) and lowest in metestrus and diestrus phases (high progesterone). Tamoxifen significantly reduced contraction parameters (P < 0.001) and estradiol levels, while mifepristone notably increased contraction force (P < 0.01), elevated estradiol levels (P < 0.001), and decreased the proportion of progesterone hormone. The IF study indicated suppression of ER, PR, and GR expression following treatment with mifepristone. Docking analysis revealed that tamoxifen interacted with potassium channels and ERβ, while mifepristone showed high affinity for PR, GR, and calcium channels. These findings highlight that oviduct contractility is dynamically regulated across the estrous cycle through both receptor-mediated and potential non-receptor and non-genomic pathways involving ion channels. © 2025 the author(s)