A bihormonal model of normal sexual stimulation; the etiology of premature ejaculation.
The physiological sexual excitation is mediated both by the sympathetic and the parasympathetic nervous system. The antagonism between testosterone (Tt) and estrogens (Es) as well as the fact that the dynamics of the sexual excitation in the male are antagonistic to those in the female are nowadays well-known; hence, the hypothesis was emitted that the sympathoparasympathetic sexual excitation is bihormonal mediated, consisting in a very active sexual hormone associated with a weak antagonistic hormone. Most studies show a serotonergic (ejaculatory) involvement in premature ejaculation (PE). Nevertheless, an effective treatment of PE is rather difficult with selective serotonin reuptake inhibitor drugs and other clinical data even suggest that changes in PE actually involve at first the sexual excitation process and only secondly the ejaculation reflex.Thus, a therapeutic model for PE is set up, starting from the physiological aspects described and from the presumed pathophysiological mechanism in PE.