Hormonal regulation of K+-channel messenger RNA in rat myometrium during oestrus cycle and in pregnancy.
The dramatic enhancement of smooth-muscle excitability in the uterus which occurs at oestrus and at term in pregnant rats is closely related to increased blood oestrogen concentrations. How oestrogen alters the electrical properties of myometrial cells is unclear, although electrical coupling between cells has been shown to increase. Many examples are known of changes in cellular excitability involving modification of existing ion channels by second-messenger pathways. Steroid hormones, in contrast, are generally thought to influence cellular processes mainly through effects on gene expression, inducing the synthesis of new proteins. Previous work, using an oocyte translation system, has shown that a very slowly activating, voltage-dependent K+ current can be expressed from the poly(A)+ RNA of oestrogen-treated rat uteri. We report here that the messenger RNA species producing this channel is rapidly and reversibly induced in the presence of oestrogen, as shown by the appearance and disappearance of this mRNA during the oestrous cycle, its emergence at the end of pregnancy, and its presence or absence following hormonal treatments. These results suggest that oestrogen controls the expression of a voltage-dependent ion channel in uterine smooth muscle cells.
D000818:Animals; D004971:Estrus / Q000502:physiology*; D005260:Female; D007473:Ion Channels / Q000378:metabolism*; D008564:Membrane Potentials; D009215:Myometrium / Q000502:physiology*; D009865:Oocytes / Q000502:physiology; D010052:Ovariectomy; D011188:Potassium / Q000378:metabolism*; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000502:physiology*; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism*; D051381:Rats; D014981:Xenopus
D007473:Ion Channels; D012333:RNA, Messenger; D011188:Potassium