Men's Health Encyclopedia: The Role of Nitric Oxide and Smooth Muscle in Healthy Erection

Nitric Oxide (NO) and Penile Erection

Penile erection is a complex neurophysiological reflex, present in infants as young as two years old. Sexual arousal can be caused by stimulation of sensory nerve endings in the genitals or by conditioned reflex stimulation of other parts of the body. These stimuli are transmitted via afferent nerves to the spinal cord and brain center. After a series of nerve cell activities, the resulting sexual arousal signals are transmitted via efferent nerves through the spinal cord to the effector organs—the external genitalia—causing a series of hemodynamic changes in the corpora cavernosa of the penis, completing the penile erection process.

The ability of the penis to erect is controlled by the parasympathetic nervous system. When the parasympathetic nervous system is excited, it releases neurotransmitters that promote the dilation of penile arteries, causing complete dilation of the penile arteries and afferent arterioles. This significantly increases blood flow into the penis. Simultaneously, these neurotransmitters bind to receptors on the epithelial cells of the cavernous sinus, causing the endothelial cells to produce large amounts of nitric oxide (NO). This NO diffuses into the adjacent smooth muscle cells, causing them to relax. Under the traction of the dilated smooth muscle cells, the cavernous sinus expands, increasing blood flow and pressure, thus blocking the subtunic and intersinus veins from completing the erection process. When NO levels decrease, the smooth muscle cells contract, the sinus space shrinks, pressure on the subtunic veins decreases, venous return increases, and penile flaccidity occurs.

A fascinating experiment was conducted where a piece of smooth muscle tissue was peeled from the corpora cavernosa of a rabbit's penis. Electrodes were connected to the nerves in the smooth muscle tissue, and after applying an electric current, the smooth muscle cells relaxed. The NO content in the smooth muscle cells was then measured. The results showed that the NO content in the relaxed smooth muscle cells was significantly higher than that in the unrelaxed smooth muscle tissue, indicating that NO plays an important role in the expansion of smooth muscle cells. Currently, many experts are researching the use of NO to treat erectile dysfunction, and have achieved good results. Some researchers have injected the NO intermediate Nicorandil into the corpora cavernosa of the penis, producing satisfactory erectile function. After injection, NO is immediately released, stimulating the erectile process. This effect of promoting erection is far greater than that of other vasoactive drugs (such as papaverine, prostaglandin E, and phentolamine). Many experts believe that with further research into the role of NO in penile erection, new breakthroughs will be achieved in the treatment of erectile dysfunction.

The Role of Smooth Muscle Cells in Penile Erection

Increased pressure within the cavernous sinuses is crucial for penile erection. How does this pressure increase? Previous research suggested that the increased pressure primarily depended on the dilation of penile arteries and the contraction of penile veins. However, recent studies have found that the pressure within the cavernous sinuses during penile erection in adults is several to ten times higher than that in the arteries of the limbs. Such high pressure cannot be achieved by a single vascular factor. Therefore, it is believed that smooth muscle cells in the erectile tissue play a vital role in this process. As mentioned earlier, smooth muscle cells function under the control of the sympathetic and parasympathetic nervous systems. As early as 1979, Professor Joann McConell of the Texas Medical School discovered that stimulating the parasympathetic nervous system in animals causes relaxation of the smooth muscle cells in the corpora cavernosa, widening the cavernous sinus space, increasing cavernous sinus pressure and penile erection rigidity. Conversely, stimulating the sympathetic nervous system causes smooth muscle cell contraction, narrowing of the cavernous sinuses, decreased intrasquamous pressure, and penile flaccidity. In 1989, Robet proposed that relaxation of smooth muscle cells in penile erectile tissue primarily dilates the spiral arteries of the penis and expands the cavernous sinus space, promoting erection. Literature reports that the number of smooth muscle cells in the corpus cavernosum of the penis is significantly reduced in patients with erectile dysfunction, accounting for only 10%–36% of the erectile tissue, compared to 40%–60% in normal individuals.

Recently, Dimitrios G. Hatzichris-tau et al. published an article in the American Journal of Urology in 1995, pointing out that relaxation of smooth muscle cells in the corpus cavernosum is an important factor in the obstruction of penile venous return and sustained penile erection. Rapid penile venous return and weak erection are caused by incomplete relaxation of smooth muscle cells in the corpus cavernosum. It has been reported that if the smooth muscle cells in the corpus cavernosum undergo pathological changes and cannot maintain normal relaxation and contraction functions, even with normal local nerve function and blood supply, it is difficult to maintain normal penile erection. This is an important reason why some patients with vascular erectile dysfunction still cannot restore normal erectile function after penile angioplasty. Therefore, a penile cavernous body biopsy should be performed before performing penile angioplasty on patients with erectile dysfunction to understand the pathological changes in the penile cavernous body tissue and smooth muscle cells. If the number of smooth muscle cells is significantly reduced and there is a large amount of fibrous tissue hyperplasia, penile angioplasty is not suitable, and penile prosthesis implantation should be chosen instead. Otherwise, it will be difficult to achieve satisfactory treatment results after surgery.