Effects of ovarian hormone treatment on Ca(2+)-induced contractions and Ca(2+)-antagonism in the depolarized rat myometrium.

M G Zeitune, P M Bazerque
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Abstract

The effects of estrogen (E), progesterone (P) and estrogen plus progesterone (E+P) treatment on Ca-induced contraction in the KCL-depolarized uterine muscle, and the influences on the Ca2+ antagonism induced by reserpine and verapamil "in vitro" were studied. Uterine muscles from rats in estrus were taken as controls. Uteri from spayed untreated rats showed the same sensitivity to Ca2+ as those from estrus rats, but castration decreased maximal contractile tension to Ca2+ and Ca2+ threshold. P treatment failed to modified the effects of castration on the responses to Ca2+. E or E+P treatments decreased the sensitivity to Ca2+ but only E+P increased slope values and maximal contractile tension. E and E+P increased the potency of verapamil Ca2+ antagonism but none of the treatments modified reserpine direct inhibitory effects. The results obtained suggest that alterations on uterine contractility by hormone treatment are the result of complex interactions between both genomic effects on the contractile process as well as non-genomic direct actions of the hormones on Ca2+ membrane permeability.

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卵巢激素治疗对去极化大鼠肌层Ca(2+)诱导的收缩和Ca(2+)拮抗作用的影响。
研究了雌激素(E)、黄体酮(P)和雌激素+黄体酮(E+P)处理对kcl -去极化子宫肌ca诱导收缩的影响,以及利血平和维拉帕米对体外Ca2+拮抗的影响。以发情期大鼠子宫肌为对照。未阉割的大鼠子宫对Ca2+的敏感性与发情大鼠相同,但阉割降低了Ca2+的最大收缩张力和Ca2+阈值。P处理未能改变去势对Ca2+反应的影响。E或E+P处理降低了对Ca2+的敏感性,但只有E+P处理增加了斜率值和最大收缩张力。E和E+P增加了维拉帕米对Ca2+的拮抗作用,但没有一种治疗改变利血平的直接抑制作用。这些结果表明,激素治疗对子宫收缩性的改变是基因组对收缩过程的影响以及激素对Ca2+膜通透性的非基因组直接作用之间复杂相互作用的结果。
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