An erection
is produced during sexual arousal due to the filling
of the corpora cavernosa and corpus spongiosum of the
penis with blood. The arteries of the penis relax while
the veins constrict, allowing the penis to hold onto
a large amount of blood. Prostate cancer treatment may
result in impotence due to the arteriosclerosis or diversion
of the blood flow to the penis or damage to the nerves.
Chemically, the body produces erection by releasing
nitric oxide from nerve cells called NANC. The nitric
oxide turns on the production of an enzyme, guanylate
cyclase, which converts guanosine triphosphate (GTP)
into cyclic guanosine monophosphate (cGMP). Cyclic guanosine
monophosphate causes the smooth muscles of the arterial
walls in the penis to relax and allow blood to flow
in; however, a enzyme called phosphodiesterase type
5 (PDE 5), breaks down cGMP and the arterial walls stop
relaxing. Prostate cancer treatment can cause impotence
due to therapies that interfere with the physiological
and chemical process involved in producing and maintaining
erection.
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