Figure 2131

Photomicrograph of corpus spongiosum, a. This photomicrograph of a H&E-stained section shows the corpus spongiosum and urethra. x20. b. This higher magnification of the corpus spongiosum shows the numerous irregularly shaped vascular spaces. Note the surrounding layer of smooth muscle (SM) forming the "subendothelial cushions." X135.

Erection of the penis is a vascular event initiated by the CNS and maintained by complex interactions between vascular and neurologic events. The CNS responds to external and/or internal stimuli (sensory impulses, perception, desire, etc.) that involve the sympathetic and parasympathetic innervation of the penis.

Parasympathetic stimulation initiates erection by relaxation of the trabecular smooth muscle cells and dilation of the helicine arteries. This leads to expansion of the corpora cavernosa and, to a lesser degree, the corpus spongiosum. Arterial blood accumulates in these erectile tissues by compression of the venules against the nondistendible tunica albugínea. This process is referred to as the corporal veno-occlusive mechanism. The tunica albugínea also compresses the larger veins that drain blood from the corpora cavernosa so that venous outflow is also blocked, resulting in tumescence and rigidity of the penis.

Two neuromediators, acetylcholine and nitric oxide, are involved In the relaxation of smooth muscle during the initiation and maintenance of penile erection.

• Acetylcholine is released by the parasympathetic nerve endings and acts primarily on the endothelial cells that line the vascular spaces of the corpora cavernosa. This causes the release of vasoactive intestinal peptide (VIP) and, more importantly, nitric oxide.

• Nitric oxide (NO) activates guanylate cyclase in the trabecular smooth muscle cells to produce cyclic guanosine monophosphate (cGMP). cGMP causes the smooth muscle cells to relax.

Sympathetic stimulation terminates penile erection by causing contraction of the trabecular smooth muscle cells of the helicine arteries. These events decrease the flow of blood to the corpora cavernosa, reducing blood pressure in the erectile tissue to normal venous pressure. The lower pressure within the corpus caver-nosum allows the veins leading from the corpora cavernosa to open and drain the excess blood.

Erectile dysfunction is an inability to achieve and maintain sufficient penile erection to complete satisfactory intercourse. Adequate arterial blood supply is critical for erection, therefore any disorder that decreases blood flow into the corpora cavernosa may cause erectile failure.

Many cases of erectile dysfunction that do not involve parasympathetic nerve damage can now be treated effectively with sildenafil citrate (Viagra). This compound enhances the relaxing effect of NO on smooth muscle cells of the corpora cavernosa by inhibiting phosphodiesterase, which is responsible for degradation of cGMP. As noted above, cGMP causes smooth muscle relaxation, which in turn allows inflow of blood into the corpus cavernosum to initiate erection. However, when parasympathetic nerve damage has occurred (e.g., as a complication of prostatic surgery), sildenafil citrate will have no effect because the event involving parasympathetic stimulation and release of acetylcholine cannot occur. Without acetylcholine, NO cannot produce cGMP. Without cGMP, smooth muscle cells cannot relax to allow inflow of blood to fill the erectile tissue.

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