Ayar A, Kutlu S, Yilmaz B, Kelestimur H
Department of Pharmacology, Firat University, Faculty of Medicine, Elazig, Turkey.
Neuro Endocrinol Lett. 2001 Jun;22(3):199-207.
The aim of this study was to investigate the effects of melatonin on spontaneous and oxytocin-induced contractility of pregnant and non-pregnant rat myometrium in vitro.
Myometrial strips were removed from virgin or late pregnant (21 days gestation) Wistar rats following decapitation and placed in an organ bath containing Krebs' solution at 37 degrees C and pH 7.4, constantly bubbled with 95% oxygen-5% carbon dioxide and isometric contractions were recorded. Effects of cumulative concentrations of melatonin (0.1 to 10 microM) on spontaneous and oxytocin-induced contractions were studied. Possible involvement of Ca(2+)-activated K (+) channels in inhibitory actions of melatonin was investigated by using apamin (100 nM).
Melatonin inhibited spontaneous and oxytocin-induced contractions of myometrium from both virgin and late pregnant rats in a dose-dependent manner. After inhibition of oxytocin-induced contractions by melatonin, application of prostaglandin F (2alpha) (1 microM) but not high KCl (30 mM) containing solution initiated contractile activity. Inhibitory response induced by melatonin (13 microM) was not affected by apamin (100 nM).
Data from this study demonstrates that melatonin inhibits spontaneous and oxytocin-induced contractions of myometrium from pregnant and non-pregnant rats. Although the exact mechanism is not clear, melatonin-induced inhibition of myometrial contractions may results from its interactions with Ca(2+) channels.
本研究旨在探讨褪黑素对体外培养的妊娠和未妊娠大鼠子宫肌层自发性收缩及催产素诱导收缩的影响。
断头处死未孕或妊娠晚期(妊娠21天)的Wistar大鼠,取出子宫肌条,置于含 Krebs 溶液的器官浴槽中,37℃恒温,pH 7.4,持续通入95%氧气-5%二氧化碳,记录等长收缩。研究褪黑素累积浓度(0.1至10微摩尔)对自发性收缩及催产素诱导收缩的影响。使用蜂毒明肽(100纳摩尔)研究Ca(2 +) 激活的K(+) 通道在褪黑素抑制作用中的可能参与情况。
褪黑素以剂量依赖方式抑制未孕和妊娠晚期大鼠子宫肌层的自发性收缩及催产素诱导的收缩。褪黑素抑制催产素诱导的收缩后,应用前列腺素F(2α)(1微摩尔)而非含高钾(30毫摩尔)的溶液可引发收缩活性。褪黑素(13微摩尔)诱导的抑制反应不受蜂毒明肽(100纳摩尔)影响。
本研究数据表明,褪黑素抑制妊娠和未妊娠大鼠子宫肌层的自发性收缩及催产素诱导的收缩。尽管确切机制尚不清楚,但褪黑素诱导的子宫肌层收缩抑制可能源于其与Ca(2 +) 通道的相互作用。