Waldegger S, Lang U, Herzer T, Suessbrich H, Binder K, Lepple-Wienhues A, Nagl U, Paulmichl M, Franz H B, Kiesl L, Lang F, Busch A E
Institute of Physiology, Eberhard-Karls-Universität Tübingen, Germany.
Naunyn Schmiedebergs Arch Pharmacol. 1996 Dec;354(6):698-702. doi: 10.1007/BF00166894.
Previously it was shown that minK protein expression in uterus is regulated by estrogen. In the present study, we were interested in putative direct effects of estrogen on minK protein induced K+ currents (IminK) in Xenopus oocytes. Superfusion with 17-beta-estradiol (1 microM) resulted in an inhibition of minK-induced currents, but had no appreciable effects on the delayed rectifier and inward rectifier K+ channels Kv1.1 and Kir2.1, respectively. The inhibition of IminK by 17-beta-estradiol was concentration-dependent, with an IC50 of approximately 0.5 microM. In the presence of 17-beta-estradiol, the conductance-voltage relationship was shifted to more depolarized potentials. IminK inhibition occurred also in the presence of the estrogen-receptor antagonist tamoxifen, suggesting that a mechanism independent of estrogen receptors is involved. The synthetic estrogen diethylstilbestrol (DES) also inhibited IminK but with a lower affinity (IC50 of 4.5 microM), while cortisol and progesterone had only weak effects on IminK. In summary, the results indicate that estrogens directly inhibit IminK.
先前的研究表明，子宫中minK蛋白的表达受雌激素调控。在本研究中，我们关注雌激素对非洲爪蟾卵母细胞中minK蛋白诱导的钾离子电流（IminK）的假定直接作用。用17-β-雌二醇（1微摩尔）灌流导致minK诱导电流受到抑制，但对延迟整流钾通道和内向整流钾通道Kv1.1和Kir2.1分别没有明显影响。17-β-雌二醇对IminK的抑制作用呈浓度依赖性，半数抑制浓度（IC50）约为0.5微摩尔。在存在17-β-雌二醇的情况下，电导-电压关系向更去极化的电位偏移。在雌激素受体拮抗剂他莫昔芬存在的情况下，IminK也受到抑制，这表明涉及一种独立于雌激素受体的机制。合成雌激素己烯雌酚（DES）也抑制IminK，但亲和力较低（IC50为4.5微摩尔），而皮质醇和孕酮对IminK只有微弱影响。总之，结果表明雌激素直接抑制IminK。
