Regulation of epididymal contractility during semen emission, the first part of the ejaculatory process: a role for estrogen.
BACKGROUND
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.


OBJECTIVE
This article reviews some of the physiological non-neuronal mechanisms underlying the epididymal contractility, and reports evidences of an estrogenic regulation.


METHODS
We reviewed here our and other groups' publications on the role of ET-1/OT and estrogens in modulating the epididymal contractility.


METHODS
Data were obtained by an extensive examination of the published peer-reviewed literature on this topic.


RESULTS
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.


CONCLUSIONS
Ejaculation is the result of the complex, and today still not fully elucidated, interplay between neuronal and non-neuronal, sex-steroid-dependent factors.
Vignozzi
Linda
L
University of Florence-Clinical Physiopathology, Andrology Unit, Florence, Italy.
Filippi
Sandra
S
Morelli
Annamaria
A
Luconi
Michaela
M
Jannini
Emmanuele
E
Forti
Gianni
G
Maggi
Mario
M
D000818:Animals; D019898:Autocrine Communication / Q000502:physiology; D004542:Ejaculation / Q000502:physiology*; D019332:Endothelin-1 / Q000502:physiology; D004822:Epididymis / Q000294:innervation / Q000502:physiology*; D004967:Estrogens / Q000502:physiology*; D006801:Humans; D008297:Male; D009119:Muscle Contraction / Q000502:physiology*; D009948:Orgasm / Q000502:physiology; D010121:Oxytocin / Q000502:physiology; D019899:Paracrine Communication / Q000502:physiology; D010275:Parasympathetic Nervous System / Q000502:physiology; D010525:Peripheral Nerves / Q000502:physiology; D011817:Rabbits; D017466:Receptors, Endothelin / Q000502:physiology; D018045:Receptors, Oxytocin / Q000502:physiology; D012661:Semen / Q000502:physiology*; D013116:Spinal Cord / Q000502:physiology; D013564:Sympathetic Nervous System / Q000502:physiology; D014521:Urethra / Q000294:innervation; D014649:Vas Deferens / Q000502:physiology
D019332:Endothelin-1; D004967:Estrogens; D017466:Receptors, Endothelin; D018045:Receptors, Oxytocin; D010121:Oxytocin