Levin R J, Phillips J C
J Physiol. 1983 Mar;336:465-78. doi: 10.1113/jphysiol.1983.sp014591.
The transuterine potential difference (p.d.) generated by the endometrium was measured in vivo in anaesthetized, ovariectomized rats treated with 10 micrograms oestradiol-17 beta each day for 3 days. Intravenous injection of adrenaline induced transient hyperpolarization of the p.d.; sigmoid dose-dependency was observed over the range 2-40 micrograms/kg. Pre-treatment of the rats with syrosingopine shifted the dose-response curve to the left (enhancement) while combined propranolol (800 micrograms/kg) and phentolamine (800 micrograms/kg) shifted the dose-response curve to the right (depression). Isoprenaline gave similar quantitative changes in the p.d. in vivo which displayed a similar time course and sigmoid dose-dependency. Propranolol alone (800 micrograms/kg) shifted this dose-response curve significantly to the right. Addition of adrenaline or isoprenaline to the serosal solution bathing uteri incubated in vitro after removal from oestradiol-treated rats induced changes in endometrial bioelectric activity that exhibited sigmoid dose-response curves for the transuterine p.d. and short-circuit current (Isc). Propranolol significantly shifted the dose-response curves for adrenaline to the right. Only adrenaline caused small but significant decreases in the uterine resistance but these were not dose-dependent. Acetylcholine, 5-hydroxytryptamine, noradrenaline and phenylephrine had no effect on the transuterine p.d. in vivo or in vitro or on the Isc in vitro. No significant electrical changes could be induced by adrenaline or any of the other drugs across the uteri from untreated ovariectomized rats either in vivo or in vitro. The transluminal membrane p.d. of surface endometrial cells measured with micro-electrodes was depolarized by an addition of serosal adrenaline but only 41% of the cells successfully impaled responded in this way. The results indicate that endometrial cells under oestrogen stimulation possess electrogenic processes that can be modulated specifically by adrenaline through the mediation of a serosally sited beta-adrenoceptor. The physiological role of the mechanism has yet to be established.
在对麻醉的、卵巢切除的大鼠进行体内实验时，测量了子宫内膜产生的经子宫电位差（p.d.）。这些大鼠每天接受10微克的β-雌二醇治疗，持续3天。静脉注射肾上腺素会引起电位差的短暂超极化；在2 - 40微克/千克的范围内观察到了S形剂量依赖性。用蛇根碱对大鼠进行预处理会使剂量反应曲线向左移动（增强作用），而联合使用普萘洛尔（800微克/千克）和酚妥拉明（800微克/千克）会使剂量反应曲线向右移动（抑制作用）。异丙肾上腺素在体内也会使电位差产生类似的定量变化，且呈现出相似的时间进程和S形剂量依赖性。单独使用普萘洛尔（800微克/千克）会使该剂量反应曲线显著向右移动。从接受雌二醇治疗的大鼠身上取出子宫后，在体外培养时，向浸泡子宫的浆膜溶液中添加肾上腺素或异丙肾上腺素会引起子宫内膜生物电活动的变化，这些变化呈现出经子宫电位差和短路电流（Isc）的S形剂量反应曲线。普萘洛尔会使肾上腺素的剂量反应曲线显著向右移动。只有肾上腺素会使子宫电阻出现小幅度但显著的降低，但这些降低并不依赖于剂量。乙酰胆碱、5-羟色胺、去甲肾上腺素和苯肾上腺素在体内或体外对经子宫电位差或体外短路电流均无影响。无论是在体内还是体外，肾上腺素或任何其他药物都不会在未处理的卵巢切除大鼠的子宫上引起明显的电变化。用微电极测量表面子宫内膜细胞的跨腔膜电位差时，添加浆膜肾上腺素会使其去极化，但只有41%成功刺入的细胞会有这种反应。结果表明，在雌激素刺激下的子宫内膜细胞具有电生成过程，该过程可通过浆膜上的β-肾上腺素能受体介导，由肾上腺素进行特异性调节。该机制的生理作用尚待确定。
