Abstract
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.
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