It is now well established that oxytocin is present in the mammalian testis and there is growing evidence that the peptide plays a role in the male reproductive tract by both assisting sperm transport and modulating steroidogenesis. In the testis, oxytocin has been shown not only to modulate testosterone production but also to increase the activity of the enzyme 5 alpha-reductase which converts testosterone to dihydrotestosterone (DHT). The prostate is an androgen-dependent organ with DHT being the active steroid. Oxytocin is present in the mammalian prostate. We have shown in the rat that levels of the peptide can be regulated by androgens, prostatic oxytocin concentrations being decreased by testosterone and increased following castration or treatment with an antiandrogen. Oxytocin treatment increases 5 alpha-reductase activity in the prostate of healthy young rats but, unlike the testis, this rise in enzyme activity is only transient. We thus propose that a local feedback mechanism may act to control prostatic levels of DHT and hence prostatic growth. Benign prostatic hyperplasia (BPH) is a common disease which affects both men and dogs. The aetiology of the disease is complex but both DHT and aging are important factors. Oxytocin levels are raised in prostatic tissue from dogs with BPH and the increase in peptide is accompanied by increased 5 alpha-reductase activity. Preliminary findings also suggest that prostatic oxytocin levels are raised in tissue from men with BPH. These data lead us to suggest that oxytocin may be involved in the pathophysiology of the prostate gland.