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VOL. 73 (4), 963-985, 2007 PHISIOLOGY OF PENILE VASCULATURE...

INTRODUCTION

Erectile dysfunction (ED), defined as the consistent inability to
achieve and maintain a penile erection sufficient for adequate sexual
performance (1), is a predominantly vascular disease with a high
prevalence in patients with vascular disorders such as diabetes,
aging, hypercholesterolemia, hypertension, sedentary life style and
cigarette smoking (2, 3). Loss of endothelium integrity and
subsequent endothelial dysfunction during the latter pathological
conditions plays an essential role in the pathogenesis of ED.
Therefore, ED is considered as an early manifestation of systemic
endothelial dysfunction and cardiovascular disease (4).

The nitric oxide (NO) pathway is of critical importance in the
physiology of penile erection and also in the pathophysiology and
pharmacological management of ED (4-6). The constitutive
endothelial NO synthase (eNOS) and neuronal NO synthase (nNOS)
isoforms are tightly regulated and produce relevant levels of NO in
endothelial cells and autonomic nerve endings of the penis (4). Penile
erection occurs when NO released from nerve terminals and
endothelium upon sexual stimulation decreases vascular resistance
and increases blood flow through cavernous and helicine arteries.
This allows the filling of the sinoids, the rise in intracavernosal
pressure (ICP) and the restriction of venous outflow by compression
of subtunical veins against the tunica albuginea with entrapment of
pressurized blood in the corpora cavernosa, which is referred to as
veno-occlusive mechanism (5, 7, 8). ED can be considered as a three-
fold process where arterial insufficiency is followed by inability to
obtain tumescence due to deffective filling of the corpum
cavernosum (CC) and faulty veno-occlusion (9).

Penile erection and flaccidity are ultimately regulated by the
relaxation and contraction, respectively, of erectile smooth muscle,
and a metabolic imbalance between contractile and relaxant factors
in the CC, penile arterties and veins is one of the main causes of
organic ED. The present review summarizes the research work
carried out by our group for more than a decade on the mechanims
underlying the contractile/relaxant processes of the penile
vasculature, with special regard to the role of the vascular
endothelium in the phsyiology of erection, in the pathophsyiology of

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