Penile erection is a vascular phenomenon that results from smooth muscle relaxation, arterial dilation and venous restriction. The
atherosclerosis of the penis that occurs with aging causes a decrease in penile
oxygen tension. A reduction of smooth muscle cells has been demonstrated in relation with this change in
oxygen tension. Changes in the ratio of penile
collagen have also been observed and could explain the decrease in penile elasticity and compliance. Chronic
ischemia is, therefore, associated with
fibrosis but also with
nitric oxide (NO)-cyclic
guanosine monophosphate. The sensitivity of the alpha-
adrenoceptors on the smooth muscle cells increases with aging. All those modifications can explain the prevalence of
erectile dysfunction with aging. Low
oxygen tension in
prostanoid production may also play a role in the mechanism of
ischemia-induced cavernosal
fibrosis; however, intracavernous
injections of
prostaglandin E(1) do not seem to modify the intracavernous structures by reducing
muscular atrophy. The effects of
androgen on libido and sexual behavior are well established, but their role in the human erectile mechanism remains unclear. Several studies performed on animals have demonstrated impacts directly on both the physiological function and the trabecular structure of the corpora cavernosa in rats, dogs and rabbits. However, in humans, no study seems to demonstrate a role of
testosterone on
muscular atrophy or penile neurologic control.
Testosterone treatment alters the human behavior but not penile physiologic processes. Further studies are necessary to explain the real role of
testosterone not only on the peripheral mechanism of erection but also on the central control.