Batra S
Eur J Pharmacol. 1986 Aug 7;127(1-2):37-42. doi: 10.1016/0014-2999(86)90203-7.
In order to elucidate the mechanisms by which estrogen treatment increases uterine contractility, the effect of estrogen on Ca uptake was measured in the isolated rabbit uterus as well as in the urethra and urinary bladder. Estrogen treatment more than doubled the amount of cellular Ca uptake in the uterus during both rest and potassium-induced depolarization. Combined estrogen and progesterone treatment had a similar effect to estrogen alone. In both urinary bladder and the urethra, treatment with estrogen alone, or estrogen combined with progesterone had no effect on Ca uptake. Cellular Ca uptake was higher in uteri of rabbits subjected to progesterone withdrawal than in those that were under progesterone dominance. It is concluded that estrogen-induced increase in Ca entry into the uterine smooth muscle cells is a likely mechanism underlying increased uterine contractility. Since this effect of estrogen was not antagonized by progesterone, it may not strictly rely on the genomic action of estrogen. The increase in cellular calcium following progesterone withdrawal could be one of the mechanisms for the evolution of myometrial activity at parturition.
为了阐明雌激素治疗增加子宫收缩力的机制，在离体兔子宫以及尿道和膀胱中测量了雌激素对钙摄取的影响。在静息期和钾诱导的去极化过程中，雌激素治疗使子宫细胞的钙摄取量增加了一倍多。雌激素和孕激素联合治疗与单独使用雌激素有相似的效果。在膀胱和尿道中，单独使用雌激素或雌激素与孕激素联合治疗对钙摄取均无影响。孕酮撤药的兔子子宫中的细胞钙摄取高于处于孕酮优势状态的兔子。得出的结论是，雌激素诱导的子宫平滑肌细胞钙内流增加可能是子宫收缩力增加的潜在机制。由于雌激素的这种作用未被孕激素拮抗，它可能并不严格依赖于雌激素的基因组作用。孕酮撤药后细胞钙的增加可能是分娩时子宫肌层活动演变的机制之一。
