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Phosphodiesterase 5 inhibitors in the management of benign
prostatic hyperplasia and erectile dysfunction: the best of
both worlds
Peter Wong, Nathan Lawrentschuk and Damien M. Bolton
Introduction
In 1986, Caine [1] proposed that infravesical obstruction
in men with symptomatic benign prostatic hyperplasia
(BPH) comprised both static and dynamic components.
The static component of obstruction is related primarily
to the mechanical obstruction caused by the enlarging
prostatic adenoma, whereas the dynamic component is
principally determined by the tone of the prostatic
smooth muscle. Two avenues for pharmacotherapy have
therefore evolved, namely shrinking the prostate tissue or
relaxing the smooth muscle of the prostate. Medical
therapy is now first-line treatment for most men with
symptomatic benign prostatic hyperplasia [2]. Contem-
porary medical therapies are noninvasive, reversible,
cause minimal side effects, and significantly improve
symptoms [3,4]. Alpha-blockers (alpha
1
-adrenoceptor
antagonists) are first line in most instances, with 5-
alpha-reductase inhibitors, alone or in combination with
alpha-blockers, also clinically efficacious [5].
It is important to note the relationship between lower
urinary tract symptoms (LUTS) and sexual dysfunction,
with sexual dysfunction being highly prevalent in men
with LUTS [6]. By sexual dysfunction, we refer to
decreased libido, erectile dysfunction, decreased ejacula-
tion and other ejaculation disorders. This knowledge has
spurned interest in the potential use of phosphodiester-
ase 5 (PDE-5) inhibitors in the treatment of symptomatic
BPH [7,8].
Pathophysiology of lower urinary tract
symptoms and benign prostatic hyperplasia
Prostatic smooth muscle tone is under the influence of
the autonomic nervous system. Thus, any pharmacologic
agent that may affect the functioning of this system could
alter resistance in smooth muscle tone.
There are three main components to clinically significant
BPH: static, dynamic and detrusor muscle components as
outlined above. The dynamic component is associated
with an increase in smooth muscle tone of the prostate.
These smooth muscle cells contract under the influence
of noradrenergic sympathetic nerves, thereby constrict-
ing the urethra [9]. Prostatic tissue contains high levels of
both alpha
1
and alpha
2
adrenoceptors – 98% of the alpha
1
adrenoceptors are associated with stromal elements of the
prostate [10]. Thus, alpha
1
-receptor blockade relaxes
smooth muscle, resulting in relief of bladder outlet
obstruction that enhances urine flow [11]. Different
subtypes of alpha
1
receptors have been identified, with
alpha
1A
being the predominant one. Two alpha
1A
adre-
noceptors generated by genetic polymorphism have been
identified with different ethnic distributions but similar
pharmacologic properties [12].
University of Melbourne, Departments of Surgery and
Urology, Austin Hospital, Melbourne, Australia
Correspondence to Associate Professor Damien M.
Bolton, Director of Urology, Austin Health, 5/210
Burgundy Street, Heidelberg, Melbourne 3084,
Australia
Tel: +61 3 9457 4049;
e-mail: damienmb@unimelb.edu.au
Current Opinion in Urology 2009, 19:7–12
Purpose of review
Phosphodiesterase 5 (PDE-5) inhibitors are established as first-line therapy in erectile
dysfunction. There is emerging evidence that they may have a role in treating patients
with lower urinary tract symptoms (LUTS) from benign prostatic hypertrophy.
Recent findings
All three commonly used PDE-5 inhibitors (sildenafil, vardenafil and tadalafil) appear to
improve LUTS as measured by the International Prostate Symptom Score. However, to
date, no change in urinary flow rates have been demonstrated.
Summary
Erectile dysfunction and LUTS frequently coexist in men of advancing age. There
appears to be an emerging role for PDE-5 inhibitors as a treatment for both conditions.
Further studies are required to elicit the exact mechanism of action in LUTS.
Keywords
benign prostatic hypertrophy, lower urinary tract symptoms, phosphodiesterase 5
inhibitors
Curr Opin Urol 19:7–12
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0963-0643
0963-0643 ß 2009 Wolters Kluwer Health | Lippincott Williams & Wilkins DOI:10.1097/MOU.0b013e328316c357