Continuing Medical Education: Regulation of Epididymal Contractility During Semen Emission, the First Part of the Ejaculatory Process: A Role for Estrogen (CME)

Abstract

Ejaculation is an important step of the male sexual response, and consists of three separate phases: emission, ejection, and orgasm. In contrast to the erectile process, whose neurological and vascular mechanisms have been well elucidated, the pathophysiology of the ejaculatory process remains yet to be completely investigated. In humans, the emission and the ejection phases are regulated by an integrated and time-coordinated activity of the parasympathetic and sympathetic systems, which finally leads to sperm propulsion from the urethra. The first step in the ejaculatory process involves the epididymis, where a series of contractile waves begins, allowing sperm progression throughout the duct and toward the vas deferens. Interestingly, along with the complex neurological pathways, some non-neuronal factors (oxytocin [OT] and endothelin-1 [ET-1]) and sex hormones (estrogen) have been demonstrated to take part in the peripheral regulation of epididymal contractility. This article reviews some of the physiological non-neuronal mechanisms underlying the epididymal contractility, and reports evidences of an estrogenic regulation. We reviewed here our and other groups' publications on the role of ET-1/OT and estrogens in modulating the epididymal contractility. Data were obtained by an extensive examination of the published peer-reviewed literature on this topic. Evidences support that, although the epididymis has a rich innervation, other local, non-neuronal factors participate in the nerve-independent epididymal contractility. ET-1 and OT, along with their cognate receptors, have been demonstrated to act, in an estrogen-dependent autocrine and paracrine loop, to regulate epididymal contractile activity in rabbit, and at least partially, in humans. Ejaculation is the result of the complex, and today still not fully elucidated, interplay between neuronal and non-neuronal, sex-steroid-dependent factors.