Acute stimulation of a smooth muscle constrictor by oestradiol‐17β via <scp>GPER</scp>1 in bovine oviducts

<jats:title>Contents</jats:title><jats:p>Oviducts play roles in reproductive processes, including gametes transport, fertilization and early embryo development. Oviductal transport is controlled by various factors such as endothelins (<jats:styled-content style="fixed-case">EDN</jats:styled-content>s) and nitric oxide (<jats:styled-content style="fixed-case">NO</jats:styled-content>), smooth muscle contracting and relaxing factor, respectively. <jats:styled-content style="fixed-case">EDN</jats:styled-content>s and <jats:styled-content style="fixed-case">NO</jats:styled-content> production depend on an ovarian steroid hormone, oestradiol‐17β (E2) and E2 quickly exerts their biological functions through G protein‐coupled oestrogen receptor 1 (<jats:styled-content style="fixed-case">GPER</jats:styled-content>1), which mediates rapid intracellular signalling. Because follicular fluid which contains a high concentration of E2 enters the oviduct, we hypothesized that E2 in the follicular fluid participates via <jats:styled-content style="fixed-case">GPER</jats:styled-content>1 in producing <jats:styled-content style="fixed-case">EDN</jats:styled-content>s and <jats:styled-content style="fixed-case">NO</jats:styled-content>. To test this hypothesis, we investigated 1) the expression and localization of <jats:styled-content style="fixed-case">GPER</jats:styled-content>1 in bovine oviductal tissues and 2) rapid effects of E2 via <jats:styled-content style="fixed-case">GPER</jats:styled-content>1 on <jats:styled-content style="fixed-case">EDN</jats:styled-content>1, <jats:styled-content style="fixed-case">EDN</jats:styled-content>2 and inducible <jats:styled-content style="fixed-case">NO</jats:styled-content> synthase (<jats:styled-content style="fixed-case">iNOS</jats:styled-content>) expression in cultured bovine oviductal isthmic epithelial cells. <jats:styled-content style="fixed-case">GPER</jats:styled-content>1 was observed in the oviductal epithelium, stroma and smooth muscle, and its expression was highest in the isthmus. Short‐term treatments (≤1 hr) of E2 increased <jats:italic><jats:styled-content style="fixed-case">EDN</jats:styled-content>2 </jats:italic><jats:styled-content style="fixed-case">mRNA</jats:styled-content> expression in the isthmic epithelial cells, although E2 did not affect <jats:italic><jats:styled-content style="fixed-case">EDN</jats:styled-content>1</jats:italic> and <jats:italic><jats:styled-content style="fixed-case">iNOS</jats:styled-content></jats:italic> <jats:styled-content style="fixed-case">mRNA</jats:styled-content> expressions. Results of <jats:styled-content style="fixed-case">GPER</jats:styled-content>1‐selective agonist G‐1 and <jats:styled-content style="fixed-case">GPER</jats:styled-content>1‐selective antagonist G‐15 treatments revealed acute stimulation by E2, which is mediated via <jats:styled-content style="fixed-case">GPER</jats:styled-content>1. The overall findings suggested that E2 in follicular fluid rapidly stimulates <jats:styled-content style="fixed-case">EDN</jats:styled-content>2 expression via <jats:styled-content style="fixed-case">GPER</jats:styled-content>1 in the isthmic epithelial cells. Follicular fluid may play a role in retention of the ovulated oocyte in the end of ampulla by contracting the isthmus for successful fertilization.</jats:p>