Regulation of myometrial contraction by ATP-sensitive potassium (K(ATP)) channel via activation of SUR2B and Kir 6.2 in mouse

ATP-sensitive potassium (K(ATP)) channels are well characterized in cardiac, pancreatic and many other muscle cells. In the present study, functional expression of the K(ATP) channel was examined in non-pregnant murine longitudinal myometrium. Isometric contraction measurements and Western blot were used. K(ATP) channel openers (KCOs), such as pinacidil, cromakalim, diazoxide and nicorandil, inhibited spontaneous myometrial contractions in a reversible and glibenclamide-sensitive manner. KCOs inhibited oxytocin (OXT)- and prostaglandin F(2α) (PGF(2α))-induced phasic contractions in a glibenclamide-sensitive manner. SUR2B and Kir6.2 were detected by Western blot, whereas SUR1, SUR2A and Kir6.1 were not. These results show that pinacidl, cromakalim, diazoxide and nicorandil-sensitive K(ATP) channels exist in murine myometrium, which are composed of SUR2B and Kir6.2. Based on the modulatory effects of the K(ATP) channel on spontaneous contraction, OXT- and PGF(2α)-induced contractions, K(ATP) channels seem to play an essential role in murine myometrial motility via activation of SUR2B and Kir6.2.