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Submitted on July 29, 2003
Accepted on December 18, 2003
1 Andrology Unit, Endocrinology Unit and Clinical Biochemistry Unit Department of Clinical Physiopathology, Department of Anatomy, Histology and Forensic Medicine; Department of Pharmacology, University of Florence, 50139 Florence, Italy.
* To whom correspondence should be addressed. E-mail: m.maggi{at}dfc.unifi.it.
Oxytocin (OT) is released by the posterior pituitary during male orgasm and is supposed to participate in the ejaculatory process. We now report evidence demonstrating the presence of an OT receptor (OTR) gene (Real-time RT-PCR, Northern) and protein (immunohistochemistry, western and binding studies) expression in the rabbit and human corpus cavernosum (CC) and its possible involvement in the post-orgasmic penile detumescence. OTR is expressed in the penis in a concentration similar to that present in other portions of the male genital tract (MGT) and mediates CC contractility. OT-induced CC contractility is clearly regulated by changing sex steroid milieu. In fact we found that in a rabbit model of hypogonadotropic hypogonadism (induced by a single administration of the long-acting GnRH agonist triptorelin pamoate, 2.9 mg/Kg) OT responsiveness was strongly reduced and completely restored by estradiol valerate (3.3 mg/Kg weekly) but not by testosterone enanthate (30 mg/Kg weekly). Since we found that CC expresses both subtypes of estrogen receptors and P450 aromatase, we hypothesized a physiological role for endogenous estrogens in regulating OT responsiveness. We therefore treated adult rabbits with an aromatase inhibitor (letrozole, 2.5 mg/Kg) or with an anti-estrogen (tamoxifen, 0.25 mg/Kg) for 3 weeks. Both treatments significantly reduced CC responsiveness to OT stimulation. In conclusion, these findings indicate that OT might participate in inducing post-orgasmic penile flaccidity and a new role for estrogens in the male: regulation of CC responsiveness to OT.
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