Filippi S, Vignozzi L, Vannelli G B, Ledda F, Forti G, Maggi M
Andrology Unit, Department of Clinical Physiopathology, University of Firenze, Firenze, Italy.
J Endocrinol Invest. 2003;26(3 Suppl):82-6.
Oxytocin (OT) is a neurohypophysial hormone with overall unclear physiological functions in the male. Several studies indicated that OT has a key role in the central regulation of penile erection. In this mini-review we summarize its possible involvement in another aspect of the male sexuality: the ejaculatory process. Because OT is released by posterior pituitary at the time of orgasm, we postulate that OT might help sperm progression during ejaculation. Our recent studies indicate that OT receptors (OTR) are present in rabbit and human epididymis and mediate contractility. Accordingly, they are immuno-localized in the smooth muscle cells of the epididymis. However, they are also present in the epithelial compartment of the tubules. In epididymal epithelial cells in culture, OT induces the release of another potent stimulator of epididymal contractility, endothelin-1 (ET-1), which most probably amplifies OT-induced contraction. Sex steroids regulate the density of OTR in epididymis. In fact, in an experimental model of hypogonadotropic hypogonadism (hypo) induced in rabbits, estrogens, but not androgens, fully restored OT-induced epididymal contractility, up-regulating OTR gene and protein expression. In addition, deprivation of endogenous estrogens, by blocking their formation using the aromatase inhibitor letrozole, induced OT hypo-responsiveness comparable to that observed in hypo rabbits. These findings suggest a new function of estrogens in the male: regulation of OT responsiveness in epididymis.
催产素（OT）是一种神经垂体激素，其在男性体内的生理功能总体尚不清楚。多项研究表明，OT在阴茎勃起的中枢调节中起关键作用。在本综述中，我们总结了其在男性性行为的另一个方面——射精过程中可能发挥的作用。由于OT在性高潮时由垂体后叶释放，我们推测OT可能在射精过程中帮助精子推进。我们最近的研究表明，OT受体（OTR）存在于兔和人的附睾中并介导收缩性。相应地，它们免疫定位在附睾的平滑肌细胞中。然而，它们也存在于小管的上皮部分。在培养的附睾上皮细胞中，OT诱导另一种强效的附睾收缩刺激物内皮素-1（ET-1）的释放，ET-1很可能放大OT诱导的收缩。性类固醇调节附睾中OTR的密度。事实上，在兔诱导的促性腺激素缺乏性性腺功能减退（性腺功能减退）实验模型中，雌激素而非雄激素能完全恢复OT诱导的附睾收缩性，上调OTR基因和蛋白表达。此外，使用芳香化酶抑制剂来曲唑阻断内源性雌激素的形成，导致OT反应性降低，与性腺功能减退兔中观察到的情况相当。这些发现提示了雌激素在男性中的新功能：调节附睾中OT的反应性。
