Effects of cigarette smoking on erectile dysfunction

Abstract

Cigarette smoking is a leading cause of preventable morbidity and mortality in the United States. Although public policies have resulted in a decreased number of new smokers, smoking rates remain stubbornly high in certain demographics with 20% of all American middle-aged men smoking. In addition to the well-established harmful effects of smoking (i.e. coronary artery disease and lung cancer), the past three decades have led to a compendium of evidence being compiled into the development of a relationship between cigarette smoking and erectile dysfunction. The main physiologic mechanism that appears to be affected includes the nitric oxide signal transduction pathway. This review details the recent literature linking cigarette smoking to erectile dysfunction, epidemiological associations, dose dependency and the effects of smoking cessation on improving erectile quality.

Keywords: Erectile dysfunction; nitric oxide; smoking; smoking cessation; vascular disease.

Figure 1. Interplay of neuronal and endothelial effects on vascular relaxation

The main mediator of penile arterial relaxation is nitric oxide (NO). NO is released directly from neurons and indirectly via endothelial production. Cigarette smoke has been shown to directly inhibit both neuronal and endothelial isoforms of nitric oxide synthase (NOS). In addition, superoxide anions from cigarette smoke directly degrade NO. Rho-kinase (ROK) is upregulated in men who smoke thus activating myosin light chain (MLC) phosphatase that prevents NO-induced relaxation.