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
Erectile dysfunction—nitric oxide—smoking—
smoking cessation—vascular disease
Dr Jason R. Kovac, 12188-A North Meridian
Street, Suite 200, Carmel, IN, USA.
Tel.: +317-564-5130;
Fax: +317-564-5561;
Accepted: November 20, 2014
doi: 10.1111/and.12393
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.
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
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
, 1087–1092