Chernaeva L, Charakchieva S
Institute of Physiology, Bulgarian Academy of Sciences, Sofia.
Prostaglandins. 1991 Jun;41(6):571-83. doi: 10.1016/0090-6980(91)90062-k.
The effect of prostaglandin E2 /PGE2/ and indomethacin on 3H-noradrenaline (3H-NA) release- and on contractions-evoked by field electrical stimulation (FES) was studied in vitro in oviductal isthmus of mature rabbits (untreated and treated with estradiol). FES evoked guanethidine-sensitive contractions and calcium-dependent tritium overflow, which reflected 3H-NA overflow. Marked and concentration-dependent decrease of FES-evoked contractions by PGE2 (0.1-100 nM) was observed in both groups of animals. The inhibitory effect of PGE2 was more pronounced in estradiol treated animals (IC50 1.5 nM, n = 9) than in untreated animals (IC50 18 nM, n = 6). Indomethacin, 1 microM, induced a remarkably pronounced increase of FES-evoked contractions in estradiol treated (by 57.3 +/- 6.3%, n = 8) in comparison with untreated rabbits (21.4 +/- 3.8%, n = 7). The amount of FES-evoked release of tritium was significantly higher in untreated than in estradiol treated rabbits. PGE2 decreased and indomethacin increased tritium-evoked release. The effects of PGE2 and indomethacin on tritium-evoked release showed no estradiol dependence. The competitive results of PGE2 and indomethacin on both evoked contraction and 3H-NA release suggest that endogenous prostaglandin E2 takes part in modulation of adrenergic mediated contraction and that estradiol enhanced the prostaglandin effect.
在体外研究了前列腺素E2（PGE2）和吲哚美辛对成熟兔（未处理及经雌二醇处理）输卵管峡部电场刺激（FES）诱发的3H-去甲肾上腺素（3H-NA）释放及收缩的影响。FES诱发了胍乙啶敏感的收缩和钙依赖性的氚溢出，后者反映了3H-NA的溢出。在两组动物中均观察到PGE2（0.1 - 100 nM）对FES诱发的收缩有显著且浓度依赖性的降低作用。PGE2的抑制作用在经雌二醇处理的动物中（IC50 1.5 nM，n = 9）比未处理的动物中（IC50 18 nM，n = 6）更明显。与未处理的兔子（21.4 +/- 3.8%，n = 7）相比，1 microM的吲哚美辛使经雌二醇处理的兔子（n = 8）中FES诱发的收缩显著增加（57.3 +/- 6.3%）。未处理的兔子中FES诱发的氚释放量显著高于经雌二醇处理的兔子。PGE2降低而吲哚美辛增加氚诱发的释放。PGE2和吲哚美辛对氚诱发释放的作用未显示出对雌二醇的依赖性。PGE2和吲哚美辛对诱发的收缩及3H-NA释放的竞争性结果表明，内源性前列腺素E2参与了肾上腺素能介导的收缩调节，且雌二醇增强了前列腺素的作用。
