Evidence for the regulation of prostatic oxytocin by gonadal steroids in the rat

Citation
L. Jenkin et Hd. Nicholson, Evidence for the regulation of prostatic oxytocin by gonadal steroids in the rat, J ANDROLOGY, 20(1), 1999, pp. 80-87
Citations number
32
Categorie Soggetti
da verificare
Journal title
JOURNAL OF ANDROLOGY
ISSN journal
01963635 → ACNP
Volume
20
Issue
1
Year of publication
1999
Pages
80 - 87
Database
ISI
SICI code
0196-3635(199901/02)20:1<80:EFTROP>2.0.ZU;2-9
Abstract
Oxytocin and its receptor are present in the mammalian prostate, and the pe ptide has been shown to increase prostatic growth. 5 alpha-reductase activi ty, and contractility; This study was performed to investigate whether loca l concentrations of the peptide were regulated by gonadal steroids in order to establish whether oxytocin has a physiological role in the prostate. Bo th intact and castrated adult Wistar rats were treated daily for 7 days wit h either testosterone propionate or the antiandrogen cyproterone acetate. A nimals were then killed, and plasma hormone and prostatic oxytocin concentr ations were measured. A separate group of rats was treated with the 5 alpha -reductase inhibitor finasteride to investigate whether testosterone or dih ydrotestosterone (DHT) was involved in regulating oxytocin concentrations. In a further series of experiments, rats were treated with diethylstilbestr ol (DES) or the antiestrogen tamoxifen. Treatment with testosterone signifi cantly decreased prostatic oxytocin, whereas reduction of androgens by cast ration or by administration of cyproterone acetate increased prostatic pept ide concentrations without altering circulating levels of the peptide. Trea tment with finasteride increased plasma testosterone but decreased DHT conc entrations. Prostatic oxytocin concentrations were higher in finasteride-tr eated animals than in control animals with comparable testosterone levels. The data suggest that both testosterone and DHT are capable of decreasing p rostatic oxytocin concentrations. Treatment with DES did not significantly alter prostatic oxytocin, but administration of tamoxifen decreased concent rations of the peptide, suggesting that low levels of estrogen may be neces sary far oxytocin production. These data provide evidence that oxytocin is regulated by androgens, and we hypothesize that this regulatory mechanism m ay be involved in controlling prostatic growth.