Physiology of Penile Erection

Physiology of Penile Erection

Penile erection is a complex physiologic process that occurs through a coordinated interaction between the nerves, the blood vessels and the hormones.

In the flaccid penis, a balance exists between blood flow in and out of the erectile bodies.

American Academy of Family Physicians Diagnostic Evaluation of Erectile Dysfunction

Mechanics of erection. (A) In the flaccid state, arterial vessels are constricted and venous vessels are noncompressed. (B) On erection, smooth muscle relaxation in the trabeculae and arterial vasculature results in increased blood flow, which rapidly fills and dilates the cavernosal spaces. Venous outflow drops as the expanding cavernosal spaces compress the venous plexus and the larger veins passing through the tunica albuginea.

When a man gets sexually aroused, the nerves trigger a series of events which leads to the release of a substance of called nitric oxide (NO). This leads to a series of biochemical reactions ending in the increased formation of a substance called cyclic guanosine monophosphate or cGMP for short.

cGMP causes the the smooth muscles in the erectile tissues of the penis to relax and the blood flow into the corpora cavernosa increases tremendously. The rapid filling of the cavernosal spaces compresses venules resulting in decreased venous outflow, a process often referred to as the corporeal veno-occlusive mechanism. The combination of increased inflow and decreased outflow rapidly raises intracavernosal pressure resulting in progressive penile rigidity and full erection.

Mechanism of erection

Nerves and vascular endothelium release nitric oxide in response to sexual arousal, which activates cytoplasmic guanylate cyclase, converting GTP into cGMP. The increased levels of cGMP, result in cavernosal smooth muscle relaxation, dilatation of cavernosal and helicine arteries and engorgement of lacunar spaces. The expanding lacunar spaces compress the subtunical venous plexus against the tunica albuginea, decreasing cavernosal venous outflow, increasing intracavernosal pressure, with resulting penile rigidity.

GTP=guanosine triphosphate; GMP=guanosine monophosphate; cGMP=cyclic guanosine monophosphate.

This sequence after sexual arousal leading to an erection is also beautifully depicted below

Mechanism of erection

Cyclic AMP (cAMP) and cyclic GMP (cGMP), the intracellular second messengers mediating smooth-muscle relaxation, activate their specific protein kinases, which phosphorylate certain proteins to cause opening of potassium channels, closing of calcium channels, and sequestration of intracellular calcium by the endoplasmic reticulum. The resultant fall in intracellular calcium leads to smooth-muscle relaxation. Sildenafil inhibits the action of phosphodiesterase (PDE) type 5, thus increasing the intracellular concentration of cGMP. GTP denotes guanosine triphosphate, and eNOS endothelial nitric oxide synthase.

Detumescence. After ejaculation or cessation of erotic stimuli, sympathetic tonic discharge resumes, resulting in contraction of the smooth muscles around sinusoids and arterioles. Arterial flow is diminished to flaccid levels, much of the blood from the sinusoidal spaces is expelled, and the venous channels reopen.

During the return to the flaccid state, cyclic GMP is hydrolyzed to GMP by phosphodiesterase type 5. This leads to a decrease in the cGMP levels and consequently, the smooth muscles of the erectile tissues contract. Vasoconstriction of the penile arteries and contraction of the trabecular muscle, result in reduction of arterial inflow and collapse of lacunar spaces, respectively. Contraction of the trabecular muscle causes decompression of the drainage venules from the cavernous bodies, thus allowing the blood to drain out of the lacunar spaces and resulting in the penis becoming flaccid.

Although I have tried to keep the discussion to the basics, the mechanisms leading to flaccidity or detumescence are fairly complicated as seen below.

Muscles Activity

Norepinephrine from sympathetic nerve endings, and endothelins and prostaglandin F2 from the endothelium, activate receptors on smooth-muscle cells to initiate the cascade of reactions that results in elevation of intracellular calcium concentrations and smooth-muscle contraction. Protein kinase C is a regulatory component of the calcium-independent, sustained phase of agonist-induced contractile responses.

As we saw above, the central role in the penis becoming flaccid again is the decrease in the levels of cGMP which is hydrolyzed to GMP by phosphodiesterase type 5. It is important to remember this as this where the oral drug sildenalfil citrate (the famous "Viagra") works, as we shall see later.

The key to the entire system is smooth muscle. The percent of smooth muscle dictates the ability to achieve and maintain erections. Roughly 45 percent of the cavernosal body is made up of smooth muscle.

In the flaccid state, the smooth muscle cells of the penile arteries and the corpora cavernosa are in a state of tone (contraction). Relaxation of the smooth muscle (arterial and cavernosal) causes increased inflow of blood into the lacunar spaces of the corpora cavernosa. The arterial pressure expands the relaxed trabecular walls, thus expanding the tunica albuginea with subsequent elongation and compression of the draining venules. This mechanism of veno-occlusion restricts the outflow of blood through these channels. After ejaculation or cessation of the erotic stimuli, the smooth muscle surrounding the arteries and the lacunar spaces contracts. The inflow of blood is reduced and the venous drainage of the corporeal spaces is opened, returning the penis to the flaccid state. Erection of the penis is thus a haemodynamic event under the control of the autonomic nervous system. Coordination of the neuronal activity from psychogenic stimuli occurs in the hypothalamus while reflexogenic erection involves a polysynaptic coordination in the sacral parasympathetic centres.

Schematic Diagram Of Penile Erection Schematic Diagram Of Penile Erection