Penile erection
is a neurovascular event modulated by psychological and hormonal status. Sexual
stimulation causes a release of neurotransmitters from the cavernous nerve
terminals and relaxing factors from the endothelial cells in the penis
resulting in relaxation of smooth muscle in the arteries and arterioles
supplying the erectile tissue. A several-fold increase in blood flow occurs
with a concomitant increase in compliance of the sinusoids from relaxed
cavernous smooth muscle, facilitating rapid filling and expansion of the
sinusoidal system against the tunica albuginea. The subtunical venular plexuses
are thus compressed between the trabeculae and the tunica albuginea, resulting
in almost total occlusion of venous outflow (Lue et al., 1983 and Saenz
de Tejada, et al.,1989). Blood is trapped within the corpora cavernosa,
which raises the flaccid penis to an erect state. Intracavernous pressures are
increased to approximately 100 mm Hg (the full erection phase).
During sexual
activity, the bulbocavernosus reflex is triggered thus causing the
ischiocavernosus muscles to forcefully compress the base of the blood-filled
corpora cavernosa and the penis. The penis becomes very rigid, with an
intracavernous pressure reaching several hundred mm Hg (the rigid erection
phase). During this phase, inflow and outflow temporarily cease (Ignarro et
al., 1990). Detumescence can be the result of three separate activities:
sympathetic discharge during ejaculation, breakdown of second messengers by
phosphodiesterases, or cessation of erectile neurotransmitter release. The
venous channels open with contraction of the trabecular smooth muscle therefore
expelling the trapped blood and restoring flaccidity.
The penis is
innervated by autonomic and somatic nerves. The somatic component is controlled
by the pudendal nerve, which is responsible for penile sensation and the
contraction and relaxation of the bulbocavernosus and ischiocavernosus striated
muscles. The cavernous nerves regulate the blood flow during erection and
detumescence. The sympathetic and parasympathetic nerves merge to form the
cavernous nerves in the pelvis.
The principal
neurotransmitter for penile erection is nitric oxide, which is released from
nonadrenergic-noncholinergic neurotransmission of the cavernous nerves and the
endothelium (De Groat, 1993). Nitric oxide activates cyclic adenosine monophosphate (cAMP) and cyclic
guanosine monophosphate (cGMP). cAMP and cGMP in turn activates a cAMP -
cGMP-specific protein kinase, which phosphorylates certain proteins and ion
channels, resulting in: opening of the potassium channels and
hyperpolarization; sequestration of intracellular calcium by the endoplasmic
reticulum; and inhibition of calcium channels, blocking calcium influx. The
consequence is a drop in cytosolic calcium and smooth muscle relaxation/
erection. During the return to the flaccid state, cGMP is hydrolyzed to
guanosine monophosphate by phosphodiesterase type 5. Other phosphodiesterases
are also found in the corpus cavernosum, but they do not appear to play an important
role in detumescence (De Groat, 1993).