Erectile dysfunction: expectations beyond phosphodiesterase type 5 inhibition.

In the last few years the pathophysiological mechanisms of erection have been partially clarified, and the molecular machinery of the cellular components of the corpus cavernosum (CC) has been widely investigated. Since erection is a vascular event and the penis is a vascular organ, there must be an intact endothelium for an erection to occur. The regulation of penile tumescence inside the CC involves a balance between contracting and relaxing factors which regulate the functional state of smooth muscle cells. Recent studies have highlighted the importance of new local factors (i.e. phosphodiesterases, rho-kinases and endothelins), and pharmacological agents are available in the armamentarium of the specialist which are targeted to modulate the function of those mediators of erection. It is now well understood that male erectile dysfunction (ED) is a symptom rather than a disease; for this reason in the near future both general practitioners and specialists in internal medicine would have to interplay with sexual medicine. This review is intended to give the clinician some basic concepts of the pathophysiology of erection with relevance to the clinical practice, and to discuss the newest therapeutic approaches for those patients who do not respond to the treatment with oral inhibitors of phosphodiesterase Type 5.