Introduction

Erectile dysfunction has been defined by the NIH Consensus Development Panel on Impotence as “the inability to attain and/or maintain penile erection sufficient for satisfactory sexual performance” (NIH Consensus Development Panel on Impotence 1993). Today, it is generally accepted that the pathogenesis of erectile dysfunction is multifactorial, and several emotional, physical and medical factors contribute to the degree of the dysfunction. The prevalence of erectile dysfunction increases with age, and results of various surveys indicate an overall prevalence in males aged between 30 and 80 years of approximately 20% (Shabsigh and Anastasiadis 2003; Braun et al. 2003).

Physiology of erection

Erection can be regarded as a complex neurovascular process that can be initiated by recruitment of penile afferent signals (reflexogenic erection) and by visual, acoustic, tactile, olfactory and imaginary stimuli (psychogenic erection). Several brain regions have been identified that are involved in the initiation of penile erection. The effect of testosterone on these central mechanisms is described in depth in Chapter 4.

At the penile level, the erection is determined by the contractile state of the smooth muscles. Contracted smooth muscle cells in the flaccid penis minimize the blood flow into the sinuses of the corpora cavernosa. With sexual stimulation, three hemodynamic factors are essential for achievement of erection with full tumescence and rigidity:

(1) Relaxation of cavernosal smooth muscle cells which leads to intracavernosal reduction of resistance,

(2) increased arterial inflow into the sinuses of the corpora cavernosa by relaxation of smooth muscles of the arterial vessels, and

(3) restriction of venous outflow by compression of intracavernosal and subtunical venous plexus (for review van Ahlen and Hertle 2000; Shabsigh and Anastasiadis 2003).