Endothelial dysfunction in erectile dysfunction: role of the endothelium in erectile physiology and disease.

Abstract

Erectile dysfunction (ED) is defined as the consistent inability to obtain or maintain an erection for satisfactory sexual intercourse. Basic science research on erectile physiology has been devoted to investigating the pathogenesis of ED and has led to the conclusion that ED is predominately a disease of vascular origin. The incidence of ED dramatically increases in men with diabetes mellitus, hypercholesterolemia, and cardiovascular disease. Loss of the functional integrity of the endothelium and subsequent endothelial dysfunction plays an integral role in the occurrence of ED in this cohort of men. This communication reviews the role of the vascular endothelium in erectile physiology and the influence of endothelial dysfunction in the pathogenesis of ED. Future pharmacological and gene therapy interventions to restore endothelial function may represent exciting new therapeutic strategies for the treatment of ED. Penile erection is a neurovascular phenomenon that depends upon neural integrity, a functional vascular system, and healthy cavernosal tissues (Giuliano et al, 1995). Normal erectile function involves 3 synergistic and simultaneous processes: 1) neurologically mediated increase in penile arterial inflow, 2) relaxation of cavernosal smooth muscle, and 3) restriction of venous outflow from the penis. The corpus cavernosum of the penis is composed of a meshwork of interconnected smooth muscle cells lined by vascular endothelium. Of note, endothelial cells and underlying smooth muscle also line the small resistance helicine arteries that supply blood to the corpus cavernosum during penile tumescence. Pathological alteration in the anatomy of the penile vasculature or impairment of any combination of neurovascular processes can result