Oxytocin (OT) is commonly thought to be a female hormone produced by the posterior pituitary gland, whose traditional function is to enhance uterine contractions during labor and to promote milk excretion during lactation. Nowadays, OT is found to be involved in various central and peripheral signaling pathways, mainly regulating reproductive physiology and reproductive behavior. This article reviews its role in the development of male sexual function. The OT gene is abundantly expressed in giant cell neurons in the paraventricular nucleus (PVN) and supraoptic nucleus (SON) of the hypothalamus, whose axonal nerve endings terminate in the pituitary gland and release OT in it when stimulated. Only a small percentage (0.2%) of OT neurons also release OT to the posterior pituitary and other sites such as the hippocampus. OT in circulating blood is mainly released from the axon terminals of giant cell neurons in the posterior pituitary gland. 28 minutes in the cerebrospinal fluid, but only 1-2 minutes in the peripheral circulation. In addition to the central nervous system, OT is also synthesized in peripheral tissues, such as the uterus, placenta, amnion, corpus luteum and heart, acting as an autocrine or paracrine agent. The male reproductive tract also secretes OT. Leydig cells in the testes produce OT, which is involved in the contraction of the varicocele and regulates the production of testosterone and the development of spermatozoa. The concentration of OT in the prostate is much higher than in serum, and it is now believed that OT acts as a paracrine factor that regulates the activity of 5α-reductase and participates in the pathological process of BPH. In addition, the epididymis and penile corpus cavernosum may also autocrine OT. 2. OT and penile erectile function In the 1980s, OT was found to induce penile erectile response, and in fact it is one of the strong and effective drugs to induce penile erection. OT may also be involved in the process of penile erection in humans, as the concentration of OT in the blood increases during sexual stimulation, reaching a peak during ejaculation [1, 4]. In addition D1/D2 dopamine receptor agonist apomorphine (APO) induces penile erection by activating OT neurons in the PVN. Apomorphine hydrochloride has been marketed in Europe as one of the effective oral drugs for the treatment of ED. The sensitive site for the central action of OT is the PVN, within which OT activates its own OT neurons. OT receptors (OTR) have been found to be present in the PVN. Both in vitro and in vivo experiments have demonstrated that OT excites the PVN’s own neurons and releases OT, and that electrofusion or chemical destruction of the PVN results in complete loss of OT in the central nervous system, including the spinal cord, and impaired drug-induced and non-contact erectile responses. Similar phenomena have been observed with intra-lateral ventricular injections of nacre (narogram) doses of OTR antagonists. OT binds to the OTR of the PVN’s own OT neurons and increases the inward flow of calcium ions into the neuronal cell body, while exciting its own neurons. The calcium blocker, ω-conotoxin GVIA, reduces the number of OT-induced penile erections. Calcium inward flow activates calmodulin-dependent nitric oxide synthase (NOS), and NOS eventually to NO production. The latter in turn excites OT neurons to release OT, which is released via axons to brain regions other than the hypothalamus and to the spinal cord to induce penile erection [6]. Thus, OT induces penile erection by activating NOS in PVN cells. It is well known that NO is the main neurotransmitter regulating penile erection, both centrally and peripherally, and the PVN is one of the most NOS-rich brain regions. Secondly, NOS inhibitor PVN injection decreased OT-induced erectile response, and OT antagonist intra-lateral ventricular injection inhibited penile erection induced by NO donor (e.g. SNP) PVN administration. Furthermore, OT-induced penile erection in rats was accompanied by increased NO production in their PVN [7]. As to how NO activates PVN OT neurons is still unclear, and there is no evidence that it is through the NOS-CGMP signaling pathway. There are two central penile erection neural pathways induced by OT: one is PVN-hippocampus and the other is PVN-ventral medulla oblongata and spinal cord, Chen et al [8] found that intrahippocampal injection of OT in rats resulted in an increase in intracavernosal blood (ICP), while simultaneous injection of antagonists did not respond. lumbosacral segment (L4-L6), a dose-dependent increase in intracavernosal pressure was induced. In addition, these effects were lost when the cavernous nerves were cut bilaterally. OT may activate the lumbosacral parasympathetic erectile center and induce penile erection. The OT neurons of the PVN release OT via the axons to the posterior pituitary gland, which then enters the blood circulation; the classical action of OT is to contract smooth muscle, so OT in the peripheral circulation is unlikely to induce penile erection. Blood OT has been found to increase during male sexual activity, peaking at orgasm and the onset of penile weakness, so OT may be associated with muscle contraction in the genital tract and pelvic floor during orgasm. In our recent study, we found for the first time the presence of OT receptors (OTR) in rat and human penile corpus cavernosum. Quantitative RT-PCR and Western Blot further demonstrated the presence of OTR gene and protein expression in the penile corpus cavernosum, and immunohistochemistry revealed that OTR was localized in the corpus cavernosum Immunohistochemistry revealed that OTR was localized in smooth muscle and endothelial cells. In vitro contraction experiments confirmed that OT and selective OTR agonists CThr4, Gly7OT concentration-dependent contraction of cavernous tissue strips, while selective pressor V1 and V2 receptor agonists had poor effects, and OT antagonist Atosiban completely inhibited OT contractile function in vitro, and OT (2, 6, 20, 60, 200, 600 mU) intracavernosal injection doses Dependent inhibition of erectile responses induced by electrical stimulation of the cavernous nerves and intracavernous infusions of infusional sulforaphane antagonized these responses when atosiban was pre-injected. In addition, atosiban injection alone increased the increase in ICP induced by low frequency electrical stimulation. The above results are the first to confirm the presence of OTR in the penile corpus cavernosum and to mediate the contraction of cavernous smooth muscle in vivo and ex vivo. OT in the blood increased as much as 5-fold at ejaculation and the onset of penile weakness and returned to normal levels at approximately 30 minutes, suggesting that OT may mediate penile weakness after ejaculation and a prolonged period of inactivity thereafter. In conclusion, central OT is a powerful erectogenic factor, while peripheral OT may be involved in penile weakness, especially orgasm and the post-ejaculatory period. 3. OT and ejaculatory function Ejaculation actually includes 2 separate processes: first, semen and sperm enter the prostatic urethra from the end of the epididymis, vas deferens, seminal vesicles and prostate, and second, semen is ejected from the external urethral opening. It involves the epididymis, vas deferens, ejaculatory duct, bladder neck, prostate and pelvic floor muscles. Ejaculation is mainly controlled by the sympathetic nerves (T0-L2) and somatic nerves (S2-S4) in the thoracolumbar segment. In addition, other hormones are involved in the ejaculatory process, such as adrenaline from the adrenal medulla and OT from the posterior pituitary gland. In the 1960s, male and female sheep were anastomosed in the jugular vein using the cross ciculation technique and then the seminal vesicle gland of the ram was stimulated transrectally and ewes were found to lactate, a response similar to the injection of 50-100 mU OT into the ewes, and carmi found that the intensity of contraction of the pelvic muscles of the reproductive tract during sexual activity was closely related to the blood OT concentration. In fact, blood OT peaks at ejaculation and orgasm, so OT may be involved in the ejaculatory process. We have recently studied OTR gene and protein expression in the male genital tract (MGT) of rabbits and rats, which includes testes, epididymis, seminal vesicles, vas deferens, prostate and penile corpus cavernosum, with colon, liver and cornea as negative controls and uterus and mammary gland as positive controls, and Real-time quantitative RT-PCR revealed that Western blot showed consistent results with gene expression, and a single protein band of 55 KDa was detected in all MGTs. We further investigated the ex vivo and in vivo functions of the epididymal OTR. The main function of the epididymis is to store and transport spermatozoa, and its head and body are barely innervated and rely on autonomic rhythmic contraction, while the tail is rich in nerves and contracts intermittently, so in fact the tail is mainly involved in semen excretion and ejaculation. We found that OTR was expressed throughout the human epididymis and that OT concentration-dependently mediated the contractile response of human epididymal tissue strips in vitro, in response to an OT agonist similar to that inhibited by an OTR antagonist. Immunohistochemistry showed that OTR localized to endothelial cells and smooth muscle cells in the head and body and stained strongly only smooth muscle cells in the tail. We also found that OT induced the release of endothelin-1 (EF-1), a potent smooth muscle contractile factor, from murine epididymal endothelial cells. Therefore, we suggest that the interaction of OT with EF-1 mediates non-neural autonomic rhythmic movements in the head and body of the epididymis, while in the tail, only the myotome expresses OTR, and OT increases sperm expulsion during ejaculation [13-14].Whether OT increases the expulsion of viable sperm is controversial.OT increases sperm expulsion in sheep and Holstein bulls, but has no effect in rabbits.Walch et al. observed that healthy Walch et al. observed no effect on semen parameters and ejaculation time in healthy males given 16 U of OT intranasally. We recently treated five patients with severe oligospermia with intravenous administration of OT (2.5 U) and found an increase in the number of viable spermatozoa per day without any change in ejaculate volume and no statistical difference in the total number of spermatozoa, although there was a trend towards an increase. Although OT concentration increased at ejaculation, ogawa et al. found no difference in serum OT concentration at ejaculation compared with infertile subjects. In addition, the morphological structure of the epididymis and sperm development in OT gene deficient mice did not differ from normal controls, and reproductive function was not affected. In conclusion, the regulation of OT on penile erectile function is bidirectional, in the central brain it promotes and in the cavernous body it inhibits penile erection. The central OT and OTR can be used as new targets for the development of drugs to treat ED, while intracavernosal injection of OT, if successful in clinical trials, is expected to be one of the effective drugs for the treatment of abnormal penile erection. the effect of OT on ejaculatory function and seminal fluid excretion is still controversial and needs to be continued.