An erection is fundamentally a vascular event where blood flow into the penis increases dramatically, but the entire process is precisely orchestrated by the nervous system. The brain and local nerves must work in concert to coordinate the relaxation of smooth muscle and the resulting engorgement of erectile tissue. This complex neurovascular mechanism involves a balance between signals that promote erection and those that inhibit it. Understanding this process requires identifying the specific nerves, the chemical signals they release, and the pathways that initiate the response.
The Key Nerves Controlling Erection
The innervation of the penis involves three distinct types of nerves: parasympathetic, sympathetic, and somatic. These fibers converge through the pelvic plexus, which distributes signals to the pelvic organs. Parasympathetic fibers, which initiate tumescence, originate in the sacral spinal cord segments (S2–S4) and travel via the pelvic splanchnic nerves to the pelvic plexus.
From the pelvic plexus, parasympathetic and sympathetic fibers merge to form the cavernous nerves, which directly innervate the erectile tissue. These delicate bundles run alongside the prostate, making them vulnerable to damage during pelvic surgery. Sympathetic nerves originate higher up in the thoracolumbar spinal cord (T11–L2) and are responsible for maintaining the flaccid state and promoting detumescence (reversal of the erection).
The somatic nervous system is controlled by the pudendal nerve, also arising from the sacral segments (S2–S4). This nerve is responsible for sensory input from the penis and perineum, allowing for the perception of touch. It also carries motor fibers that innervate the bulbospongiosus and ischiocavernosus muscles, which contract during the rigid phase of erection to compress the veins and increase penile pressure.
How Nerve Signals Trigger Erection
The change from a flaccid to an erect state is driven by a neurochemical cascade that causes the relaxation of smooth muscle in the penile arteries and erectile tissue. When pro-erectile signals travel down the parasympathetic cavernous nerves, a specific neurotransmitter is released into the corpora cavernosa. This primary chemical messenger is Nitric Oxide (NO), which is synthesized from the nerve terminals and also released by the endothelial cells lining the blood vessels.
Nitric Oxide rapidly diffuses into the smooth muscle cells and activates the enzyme soluble guanylate cyclase (sGC). The activation of sGC increases the production of cyclic guanosine monophosphate (cGMP), which acts as an intracellular second messenger. Increased cGMP levels trigger events that reduce intracellular calcium, causing the smooth muscle surrounding the penile arteries and sinusoids to relax.
Smooth muscle relaxation causes the arteries to dilate, allowing increased blood flow into the erectile chambers (corpora cavernosa). As the chambers fill, the pressure causes the tissue to expand and compress the small veins that normally drain blood, a process known as veno-occlusion. This trapping of blood creates the rigidity necessary for a full erection. The sympathetic nervous system reverses this process by releasing neurotransmitters like norepinephrine, which cause the smooth muscles to contract, allowing the blood to drain and the penis to return to its flaccid state.
Central and Local Control Pathways
Erection initiation occurs through two separate, though often integrated, pathways that signal the peripheral nerves. The psychogenic pathway originates in the brain in response to thoughts, fantasies, or visual stimuli. These signals travel down the spinal cord to the thoracolumbar erection center (T11 and L2), and then continue to the pelvic nerves.
This psychogenic response demonstrates the descending control of the central nervous system, requiring an intact connection between the brain and the spinal cord centers. In contrast, the reflexogenic pathway is a direct, local spinal reflex triggered by tactile stimulation of the genitals. Sensory signals from touch are transmitted via the dorsal and pudendal nerves to the sacral erection center (S2 to S4).
This pathway loops within the spinal cord, activating the parasympathetic fibers to initiate the erectile response without involving the brain. Both the psychogenic and reflexogenic pathways converge their signals onto the cavernous nerves to execute the smooth muscle relaxation and vascular changes required for tumescence. While the reflexogenic pathway can function even if the connection to the brain is severed, the psychogenic pathway requires the signal to pass through the descending spinal cord tracts.
Damage to the Nervous System and Erectile Dysfunction
Damage to any part of this neural network can lead to neurogenic erectile dysfunction, compromising the signal to initiate or maintain an erection. A common cause of peripheral nerve damage is radical prostatectomy, a surgical procedure for prostate cancer, where the cavernous nerves running close to the prostate can be injured. Even with nerve-sparing techniques, the trauma can result in temporary or permanent disruption of the nerve signals.
Systemic diseases that affect nerve health, such as diabetes mellitus, can cause neuropathy that damages the small peripheral nerves responsible for releasing Nitric Oxide. This damage interrupts the chemical communication needed for smooth muscle relaxation and blood flow. Spinal cord injury is another cause, where the resulting erectile dysfunction depends on the level and completeness of the lesion.
An injury above the sacral center (S2–S4) may preserve reflexogenic erections while abolishing the psychogenic response from the brain. Damage to the lower sacral segments can eliminate the direct reflex arc, leaving only the possibility of an incomplete psychogenic erection. Other neurological conditions, including multiple sclerosis, stroke, and Parkinson’s disease, can also disrupt the central or peripheral pathways.