¹Department of Cardiac Surgery, Bristol Heart Institute, Bristol Royal Infirmary, The University of Bristol, Bristol, UK

Correspondence: Dr JY Jeremy, Department of Cardiac Surgery, Bristol Heart Institute, Bristol Royal Infirmary, The University of Bristol, Marlborough Street, Bristol BS2 8HW, UK. E-mail: j.y.jeremy@bristol.ac.uk

Received 12 May 2006; Revised 17 July 2006; Accepted 20 July 2006; Published online 19 October 2006.

Abstract

Erectile dysfunction (ED) is a widespread condition, the incidence of which is increasing globally. ED is also indicative of underlying vasculopathy and represents a predictor of more serious cardiovascular disorders. Understanding the aetiology of ED may therefore provide invaluable pointers to the pathobiology of other cardiovascular diseases (CVDs) and syndromes. It follows, too, that therapeutic interventions that are successful in treating ED may, ipso facto, be effective in treating the early stages of conditions that include atherosclerosis, angina, plaque rupture and diabetic angiopathy. One common pathological denominator in both CVD and ED is oxidative stress, that is, the overproduction of reactive oxygen species (ROS), in particular, superoxide (O₂^-) and hydrogen peroxide (H₂O₂). In this review, therefore, we consider the aetiology and pathobiology of O₂^- in promoting ED and focus on NADPH oxidase as an inducible source of O₂^- and H₂O₂. Therapeutic strategies aimed at reducing oxidative stress to improve erectile function are also discussed.