Campos-Lara G, Caracheo F, Valencia-Sánchez A, Ponce-Monter H
Unidad de Investigación Biomédica, IMSS. México.
Arch Invest Med (Mex). 1990 Jan-Mar;21(1):71-5.
This study was designed to further characterize the sensitivity to serotonin of the isolated rat uterus. The contractile response to serotonin induced by the administration of estradiol was increased depending on the duration of estradiol-treatment, reaching the maximal contractility when ovariectomized rats were treated for 48 hours. Pretreatment with actinomycin D 1 hour before estrogen administration completely blocked estrogen-induced uterine sensitivity to serotonin. These results indicate that the sensitivity of rat uterus to serotonin in vitro induced by estradiol is a response occurring in the late phase and mediated by genomic activation. Following estradiol-administration uterine sensitivity to serotonin was similar in ovariectomized and ovariectomized-hypophysectomized rats, suggesting that in this response a pituitary factor is not required. The contractile responses to acetylcholine and oxytocin were not modified by estradiol; thus, estrogens induced specifically uterine sensitivity to serotonin. The present in vitro studies using pelanserin, a potent S2-antagonist, show that serotonin induced contractions in the rat uterus are mediated by interaction with S2-receptors, since pelanserin inhibited not-competitively the contractile response to serotonin.
本研究旨在进一步明确离体大鼠子宫对5-羟色胺的敏感性特征。给予雌二醇后，子宫对5-羟色胺的收缩反应会随着雌二醇处理时间的延长而增强，当去卵巢大鼠接受48小时的雌二醇处理时，收缩能力达到最大值。在给予雌激素前1小时用放线菌素D预处理，可完全阻断雌激素诱导的子宫对5-羟色胺的敏感性。这些结果表明，雌二醇诱导的体外大鼠子宫对5-羟色胺的敏感性是晚期发生的反应，由基因组激活介导。给予雌二醇后，去卵巢大鼠和去卵巢-垂体切除大鼠子宫对5-羟色胺的敏感性相似，这表明在这种反应中不需要垂体因子。雌二醇不会改变子宫对乙酰胆碱和催产素的收缩反应；因此，雌激素特异性地诱导子宫对5-羟色胺的敏感性。目前使用强效S2拮抗剂培兰色林进行的体外研究表明，5-羟色胺诱导的大鼠子宫收缩是通过与S2受体相互作用介导的，因为培兰色林非竞争性地抑制了对5-羟色胺的收缩反应。
