Structural and functional studies of myometrial gap junctions.
Gap junctions are believed to be sites of metabolic and electrical coupling between cells. These contacts are present between myometrial cells immediately prior to and during parturition. We report the results of studies to investigate the control and the function of myometrial gap junctions. Injection of estradiol (500 micrograms/day) with or without progesterone into immature and ovariectomized mature rats demonstrated that estradiol stimulated whereas progesterone suppressed gap junction formation. Indomethacin treatment was also shown to potentiate the action of estradiol. Also, pregnant rats treated with oestradiol developed numerous myometrial gap junctions and aborted their fetuses. These results suggest that the steroid hormones and prostaglandins may control myometrial gap junction development. Diffusion studies of 3H-2-deoxyglucose in longitudinal myometrial strips revealed a significant increase in the diffusion coefficient in delivering versus ante-partum rat tissues. This indicates that there is increased metabolic transfer during parturition when gap junctions are present. The results of these studies show that steroid hormones and prostaglandins may regulate myometrial gap junctions and that metabolic, as well as electrical coupling, of uterine smooth muscle cells increase at parturition concomitant with the development of gap junctions.
D000818:Animals; D002369:Castration; D003847:Deoxyglucose / Q000378:metabolism; D004553:Electric Conductivity; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D007365:Intercellular Junctions / Q000187:drug effects / Q000502:physiology*; D009215:Myometrium / Q000187:drug effects / Q000502:physiology*; D011247:Pregnancy; D011374:Progesterone / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D013395:Sucrose / Q000378:metabolism
D011374:Progesterone; D004958:Estradiol; D013395:Sucrose; D003847:Deoxyglucose; D007213:Indomethacin