Calcium Channel, Ca++ mobilization, and Mechanical Reactivity of Estrogen- and Progesterone-Treated Rat Uterus

Properties of [3H]nitrendipine binding, high K+- and Ca++-induced contractions and the inhibition of high K+-induced contractions by verapamil were investigated in the uterine preparations isolated from rats treated with estrogen or progesterone or both. In [3H]nitrendipine binding experiments using crude membrane fractions, treatment with estrogen alone or estrogen+progesterone significantly lowered the KD; There was very little change in the Bmax. In the Ca++-depleted, high K+-containing medium, only the progesterone-, and estrogen----progesterone-treated uteri produced contractions. The estrogen-, estrogen----progesterone-, and estrogen+progesterone-treated uteri showed decreases in concentrations of Ca++ required for the maximal contractions. In the estrogen- and estrogen+progesterone-treated uteri, the dose-response curves by verapamil were shifted to the left in a parallel manner. These findings suggest that estrogen appeared to increase the affinity of calcium channels and increase transmembrane influx of Ca++, leading to enhancement of contractions, whereas progesterone might increase the Ca++ storage in the intracellular sites.