Cigarette smoking and erectile dysfunction: focus on NO bioavailability and ROS generation.
BACKGROUND
Thirty million men in the United States suffer from erectile dysfunction (ED) and this number is expected to double by 2025. Considered a major public health problem, which seriously affects the quality of life of patients and their partners, ED becomes increasingly prevalent with age and chronic smoking is a major risk factor in the development of ED.


OBJECTIVE
To review available evidence concerning the effects of cigarette smoking on vascular changes associated with decreased nitric oxide (NO) bioavailability and increased reactive oxygen species (ROS) generation.


METHODS
We examined epidemiological and clinical data linking cigarette smoking and ED, and the effects of smoking on vascular NO bioavailability and ROS generation.


METHODS
There are strong parallels between smoking and ED and considerable evidence supporting the concept that smoking-related ED is associated with reduced bioavailability of NO because of increased ROS.


RESULTS
Cigarette smoking-induced ED in human and animal models is associated with impaired arterial flow to the penis or acute vasospasm of the penile arteries. Long-term smoking produces detrimental effects on the vascular endothelium and peripheral nerves and also causes ultrastructural damage to the corporal tissue, all considered to play a role in chronic smoking-induced ED. Clinical and basic science studies provide strong indirect evidence that smoking may affect penile erection by the impairment of endothelium-dependent smooth muscle relaxation or more specifically by affecting NO production via increased ROS generation. Whether nicotine or other products of cigarette smoke mediate all effects related to vascular damage is still unknown.


CONCLUSIONS
Smoking prevention represents an important approach for reducing the risk of ED. The characterization of the components of cigarette smoke leading to ED and the mechanisms by which these components alter signaling pathways activated in erectile responses are necessary for a complete comprehension of cigarette smoking-associated ED.
Tostes
Rita C
RC
University of Sao Paulo, Department of Pharmacology, Sao Paulo, SP, Brazil. rtostes@mcg.edu
Carneiro
Fernando S
FS
Lee
Anthony J
AJ
Giachini
Fernanda R C
FR
Leite
Romulo
R
Osawa
Yoichi
Y
Webb
R Clinton
RC
D000818:Animals; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology; D007172:Erectile Dysfunction / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D018384:Oxidative Stress / Q000502:physiology; D010410:Penile Erection / Q000502:physiology; D017382:Reactive Oxygen Species / Q000378:metabolism*; D012907:Smoking / Q000503:physiopathology*
D017382:Reactive Oxygen Species; D009569:Nitric Oxide