REVIEW ARTICLE

Effects of cigarette smoking on erectile dysfunction

J. R. Kovac

, C. Labbate

, R. Ramasamy

, D. Tang

& L. I. Lipshultz

1 Urology of Indiana, Carmel, IN, USA;

2 Department of Urology and The Center for Reproductive Medicine, Baylor College of Medicine, Houston, TX, USA

Keywords

Erectile dysfunction—nitric oxide—smoking—

smoking cessation—vascular disease

Correspondence

Dr Jason R. Kovac, 12188-A North Meridian

Street, Suite 200, Carmel, IN, USA.

Tel.: +317-564-5130;

Fax: +317-564-5561;

E-mail: jason.r.kovac@gmail.com;

JKOVAC@UROLOGYIN.COM

Accepted: November 20, 2014

doi: 10.1111/and.12393

Summary

Cigarette smoking is a leading cause of preventable morbidity and mortality in

the United States. Although public policies have resulted in a decreased num-

ber of new smokers, smoking rates remain stubbornly high in certain demo-

graphics 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 smok-

ing 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.

Introduction

Erectile dysfunction is clinically deFned as the persistent

or recurrent inability to achieve/maintain an erection suf-

Fcient for satisfactory sexual performance (NIH Consen-

sus Conference, 1993). It is a far-reaching diagnosis with

20% of all men and up to 52% of males aged 40

–

70 years

being classiFed as suffering from varying degrees of ED

(±eldman

et al.

, 1994). Increasing age has long been the

strongest association with the disease process. Because the

physiology of erection is heavily dependent on vascular

changes, many of the known cardiovascular risk factors

such as hypertension and diabetes have been associated

with the development of erectile dysfunction (Miner

et al.

, 2012). Cigarette smoking can lead to cardiovascular

dysfunction and is now established to be an independent

risk factor for the development of erectile dysfunction, a

more ominous form vascular disease. Is it possible that

quitting smoking can reverse some of the processes that

contribute to ED? If so, this should become a focused

treatment goal in the Feld of sexual medicine, irrespective

of the more global health beneFts obtained following

smoking cessation.

Physiology of erectile function

The penile corpora cavernosa are specialised spongy

vascular structures encapsulated by the envelope of

the tunica albuginea. Penile erection requires adequate

relaxation of cavernous smooth muscles and dilation of

penile arterioles allowing in²ow, and subsequent trapping

of blood, within the erectile tissue (Dean & Lue, 2005).

This process is dependent upon the parasympathetic ner-

vous system, which induces smooth muscle relaxation

allowing arterial pressure blood into the corpus caverno-

sum via the actions of nitric oxide (NO) (Rajfer

et al.

1992). NO is generated by three nitric oxide synthase

(NOS) enzyme isoforms: neuronal, endothelial and induc-

ible. The neuronal isoform appears to be the primary

mediator of physiologic erection (Burnett, 1995). Neuro-

nal NO is believed to induce erections while shear stress

also propagates the erectile response via endothelial NO.

Regardless of source, NO modulates smooth muscle cyclic

GMP to induce relaxation in a paracrine fashion. Vascu-

lar relaxation in turn allows arterial blood to Fll the cor-

pora which, by distention, creates a venous seal to

maintain erection (±ig. 1).

Molecular mechanisms associating smoking with

As mentioned above, the most well-understood signal

transduction mechanism underlying ED involves the

NO pathway. With regard to smoking, both constituent

NOS isoforms, the endothelial and neuronal variants,

have been shown to be affected by cigarette smoke.

2014 Blackwell Verlag GmbH

1087

Andrologia

2015,

, 1087–1092