Jenkin L, Nicholson H D
Department of Anatomy, School of Medical Sciences, University of Bristol, United Kingdom.
J Androl. 1999 Jan-Feb;20(1):80-7.
Oxytocin and its receptor are present in the mammalian prostate, and the peptide has been shown to increase prostatic growth, 5alpha-reductase activity, and contractility. This study was performed to investigate whether local concentrations of the peptide were regulated by gonadal steroids in order to establish whether oxytocin has a physiological role in the prostate. Both intact and castrated adult Wistar rats were treated daily for 7 days with either testosterone propionate or the antiandrogen cyproterone acetate. Animals were then killed, and plasma hormone and prostatic oxytocin concentrations were measured. A separate group of rats was treated with the 5alpha-reductase inhibitor finasteride to investigate whether testosterone or dihydrotestosterone (DHT) was involved in regulating oxytocin concentrations. In a further series of experiments, rats were treated with diethylstilbestrol (DES) or the antiestrogen tamoxifen. Treatment with testosterone significantly decreased prostatic oxytocin, whereas reduction of androgens by castration or by administration of cyproterone acetate increased prostatic peptide concentrations without altering circulating levels of the peptide. Treatment with finasteride increased plasma testosterone but decreased DHT concentrations. Prostatic oxytocin concentrations were higher in finasteride-treated animals than in control animals with comparable testosterone levels. The data suggest that both testosterone and DHT are capable of decreasing prostatic oxytocin concentrations. Treatment with DES did not significantly alter prostatic oxytocin, but administration of tamoxifen decreased concentrations of the peptide, suggesting that low levels of estrogen may be necessary for oxytocin production. These data provide evidence that oxytocin is regulated by androgens, and we hypothesize that this regulatory mechanism may be involved in controlling prostatic growth.
催产素及其受体存在于哺乳动物的前列腺中，并且已证明该肽可促进前列腺生长、提高5α-还原酶活性以及增强收缩性。本研究旨在调查该肽的局部浓度是否受性腺类固醇调节，以确定催产素在前列腺中是否具有生理作用。完整和去势的成年Wistar大鼠均每日接受丙酸睾酮或抗雄激素醋酸环丙孕酮治疗，持续7天。然后处死动物，测量血浆激素和前列腺催产素浓度。另一组大鼠用5α-还原酶抑制剂非那雄胺治疗，以研究睾酮或二氢睾酮（DHT）是否参与调节催产素浓度。在另一系列实验中，大鼠用己烯雌酚（DES）或抗雌激素他莫昔芬治疗。睾酮治疗显著降低了前列腺催产素水平，而通过去势或给予醋酸环丙孕酮降低雄激素水平则增加了前列腺肽浓度，同时未改变该肽的循环水平。非那雄胺治疗使血浆睾酮升高，但降低了DHT浓度。在睾酮水平相当的情况下，非那雄胺治疗的动物前列腺催产素浓度高于对照动物。数据表明，睾酮和DHT均能够降低前列腺催产素浓度。DES治疗未显著改变前列腺催产素水平，但给予他莫昔芬降低了该肽的浓度，表明低水平雌激素可能是催产素产生所必需的。这些数据证明催产素受雄激素调节，我们推测这种调节机制可能参与控制前列腺生长。
