Penile erection is a neurovascular event that depends on neural integrity, a functional vascular system, and healthy cavernosal tissues (1). Physiological erectile function involves three synergistic and simultaneous processes: (a) a neurogenically mediated increase in penile arterial inflow, (b) relaxation of cavernosal smooth muscle, and (c) restriction of venous out- flow from the corpora cavernosa. The corpus cavernosum of the penis is composed of a meshwork of interconnected smooth muscle cells lined by vascular endothelium. In addition, endothelial cells (ECs) and underlying smooth muscle line the small-resistance helicine arteries that supply blood to the corpora cavernosa during penile tumescence. Structural and functional alterations in the vascular tree of the corpus cavernosum or impairment of any combination of neurovascular processes can result in erectile dysfunction (ED). ED has traditionally been classified as psychogenic, organic, or a combination of these two entities. More recent data show that more than80% of ED cases have an organic basis, with vascular disease being the most common etiology (2). Although ED is a natural consequence of aging, its severity is directly related to the number and degree of vascular risk factors, such as hypertension, cigarette smoking, atherosclerosis, hypercholesterolemia, and diabetes mellitus (3) (Table 167–1). Hence, endothelial dysfunction in the penile vascular bed can lead to ED (4).

ED is defined as the consistent inability to attain or maintain an erection sufficient for satisfactory sexual intercourse (5). The Massachusetts Male Aging Study (MMAS), a substantial epidemiological survey that quantified the prevalence of ED in a noninstitutionalized population of men in the Boston suburbs (3), revealed that 52% of 1,290 men aged 40 to 70 years had some degree of ED; with almost 10% exhibiting a total absence of erectile function.