The sensitivity of rat uterus to serotonin in vitro is a late estrogenic response.

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.