How erections work: blood flow, nerves and nitric oxide, in plain language

The short version: an erection is mostly a plumbing event that the nerves switch on. Signals from the brain and spinal cord reach the penis, nerve endings there release a chemical messenger called nitric oxide, and a chain of steps relaxes the smooth muscle inside the erectile tissue. Blood flows in, gets trapped, and the veins that normally drain it are squeezed nearly shut. This page walks through each link in that chain in plain language, using the FDA drug label, the National Institutes of Health (NIH) and two peer-reviewed reviews, so that the rest of what you read about ED makes more sense. If this vocabulary is new to you, our plain-language ED glossary defines each term.

What happens in the body during an erection?

Three things happen together: the arteries widen, the spongy erectile tissue fills, and the veins are compressed so blood stays in. A physiology review by urologists at the University of California, San Francisco, explains that when the penis is soft, the smooth muscle in its erectile tissue and artery walls is held contracted, letting through only a small amount of blood. Sexual stimulation triggers nerve signals that relax that muscle. The arteries then widen and blood flow rises, the expanding spaces of the erectile tissue trap the incoming blood, and that swelling presses the small veins against the tough outer sheath (the tunica albuginea), which cuts the outflow to a minimum. The authors sum it up as “sinusoidal relaxation, arterial dilatation, and venous compression” (Dean and Lue, Urol Clin North Am 2005). Pressure inside the tissue rises until the penis is erect, and contraction of muscles at the base of the penis adds further rigidity (same source).

What part do nerves play?

Nerves start the process, and different nerves handle different jobs. The review describes two kinds of nerve supply to the penis: autonomic nerves, which work without conscious control, and somatic nerves, which carry feeling and move muscle. The autonomic fibers join to form the cavernous nerves, which run into the erectile tissue. Signals coming from the lower (sacral) spinal cord through the parasympathetic nerves are responsible for starting an erection, while signals through the sympathetic nerves from the mid to lower back are responsible for ending it. The somatic nerves carry touch and other sensations from the penis and control the muscles at its base (Dean and Lue, 2005).

The brain is part of the same system. The review names areas of the hypothalamus as integration centers for sexual function and erection, and notes that conditions affecting those areas, such as Parkinson’s disease or stroke, are often associated with ED. It also points out that the cavernous nerves run close to the prostate, bladder and rectum and “are easily damaged” during radical surgery on those organs, which is why nerve-sparing techniques were developed (same source). The NIH lists “nerve damage or disorders, such as multiple sclerosis, spinal cord injuries, and damage from pelvic surgery” among the most common conditions that can lead to ED (NIDDK, Symptoms & Causes of ED). Our guide to nerve conditions and ED covers those conditions one by one.

Why do blood vessels matter so much?

An erection depends on enough blood arriving fast enough, so anything that narrows or stiffens the arteries can affect it. The review explains that hardening of the arteries (atherosclerosis) or injury in the arteries that feed the penis can lower the pressure and flow reaching the erectile tissue, which can make an erection take longer to develop and be less firm. In most men with this kind of ED, the authors say, the reduced blood flow is “a component of the generalized atherosclerotic process,” and they list high blood pressure, high cholesterol, smoking and diabetes as common risk factors (Dean and Lue, 2005).

The lining of the blood vessels matters too. The same review says the cells lining the erectile tissue (the endothelium) release nitric oxide and other substances that affect how well the smooth muscle relaxes, and that diabetes and high cholesterol have been shown to impair that lining’s role in relaxation (same source). The NIH lists heart and blood vessel diseases such as atherosclerosis, high blood pressure and stroke among the most common conditions that can lead to ED, and says ED may be a symptom of another health problem (NIDDK). That shared ground is a reason to have ED checked, not proof that any one man’s ED comes from his heart or arteries. Our guides to ED and heart disease and to what ED can signal about your health go further.

What are nitric oxide and cGMP?

Nitric oxide is the chemical signal that starts the muscle relaxation, and cGMP is the messenger it switches on inside the muscle cells. The FDA-approved prescribing information for Viagra (sildenafil) describes the sequence: erection “involves release of nitric oxide (NO) in the corpus cavernosum during sexual stimulation.” Nitric oxide activates an enzyme called guanylate cyclase, which raises levels of cyclic guanosine monophosphate (cGMP), “producing smooth muscle relaxation in the corpus cavernosum and allowing inflow of blood.” A second enzyme, phosphodiesterase type 5 (PDE5), breaks cGMP down (VIAGRA prescribing information, section 12.1, DailyMed).

The physiology review fills in where the nitric oxide comes from: nerve endings in the erectile tissue, and the cells lining its blood vessels. Inside the muscle cells, cGMP sets off changes that lower the amount of free calcium, and with less calcium the muscle relaxes (Dean and Lue, 2005). You can think of nitric oxide as the doorbell and cGMP as the person who answers it; PDE5 is what eventually closes the door again.

Why do ED medicines still need sexual stimulation?

Because they strengthen the body’s own signal rather than creating one. The Viagra label says sildenafil “enhances the effect of NO by inhibiting phosphodiesterase type 5 (PDE5),” that it has “no direct relaxant effect” on isolated erectile tissue, and that at recommended doses it “has no effect in the absence of sexual stimulation” (VIAGRA prescribing information, section 12.1). In plain terms, the medicine slows the enzyme that clears cGMP away, so when arousal releases nitric oxide, cGMP rises higher and the muscle relaxes. If the nerve signal or the nitric oxide is missing, there is less for the medicine to work with. Our guide to how ED medications work covers the four approved PDE5 inhibitors, their limits and the safety rules that come with them.

What is venous leak?

Venous leak, also called veno-occlusive dysfunction or venogenic ED, means blood gets in but is not held in well enough, because the veins are not squeezed shut the way they should be. A review in Frontiers in Cardiovascular Medicine describes it as “incomplete relaxation of corporeal smooth muscle during arterial inflow and insufficient occlusion of venous outflow tracts” (Hoppe and Diehm, Front Cardiovasc Med 2021). The physiology review says failure of adequate venous occlusion “has been proposed as one of the most common causes” of blood-vessel-related ED (Dean and Lue, 2005).

The reviews list several ways it can arise:

• Changes in the outer sheath. Age-related changes, Peyronie’s disease, diabetes or an injury to the tunica albuginea can stop it compressing the veins properly (Dean and Lue).
• Changes in the erectile tissue. Structural changes in the tissue’s elastic fibers, smooth muscle and lining may result in venous leak (Dean and Lue).
• Muscle that does not relax fully. In an anxious man with high adrenaline tone, or when too little nerve messenger is released, the tissue may not expand enough to press the veins shut (Dean and Lue).
• Shunts after priapism surgery. Surgery to treat a prolonged erection can leave channels that let blood drain out (Dean and Lue; Hoppe and Diehm).

Hoppe and Diehm add that the mechanisms “are not yet fully understood,” and that age, diabetes, prostate removal surgery, pelvic radiation and hormone-blocking therapy “appear to be potential risk factors.” They describe how specialists confirm it, with a penile duplex ultrasound followed by tests that measure pressure inside the erectile tissue and image the veins, and they summarize treatment studies with mixed results: one meta-analysis they cite reported an average clinical success rate of 59.5% for blocking leaking veins from inside the vessels, ranging from 21.9% to 100% between studies. That figure counts partial as well as full responses, the studies defined success in different ways, and full-response rates tend to be lower. They say further studies are needed (Hoppe and Diehm, 2021). Venous leak cannot be diagnosed from symptoms alone. Losing firmness quickly can have several explanations, and testing for it is a specialist’s decision.

What makes an erection go away?

The same muscle tightens again, and the veins reopen. The review explains that norepinephrine released from sympathetic nerve endings, along with substances from the vessel lining, makes the smooth muscle contract, and that stimulating the sympathetic nerves ends an erection. In an animal study the review cites, pressure first rose briefly as the muscle contracted against the closed veins, then the venous channels slowly reopened and blood drained out (Dean and Lue, 2005). On the chemical side, the Viagra label notes that PDE5 is the enzyme responsible for breaking down cGMP, the messenger behind the muscle relaxation, in the erectile tissue (VIAGRA prescribing information, section 12.1).

How do stress and anxiety fit into the chain?

They can push on the “off” side of the system. The review notes that the brain can send both encouraging and inhibiting messages to the spinal centers that control erection. It describes two proposed ways stress-related ED can happen: the brain directly damping the spinal erection centers, and high sympathetic nerve activity or adrenaline-type hormones raising the tone of the smooth muscle so it cannot relax. It also says the old belief that most ED was psychological has given way to the view that most men with ED have a mixed condition, “either predominantly functional or predominantly physical” (Dean and Lue, 2005). The NIH lists anxiety, depression and stress among the issues that can cause ED or make it worse (NIDDK).

Where can the chain break down?

Each link can be affected, and more than one can be affected at once. The review notes that many classifications have been proposed, and describes one based on mechanism: “failure to initiate,” “failure to fill” and “failure to store.” It also covers hormonal and psychological causes, and notes that “no one cause may be involved independently” (Dean and Lue, 2005).

A list like this shows what is linked to ED across many men. It cannot tell you which link, if any, is behind changes in your own erections. Our complete guide to erectile dysfunction covers causes, diagnosis and treatment in one place.

When should you talk to a clinician?

When erection changes keep happening or bother you, because the cause is worth finding. The NIH says ED is common, affecting about 40% of men at age 40, with 70% reporting it by age 70, but that it “is not a routine part of aging” (NIDDK, Definition & Facts for ED), and that it may be a symptom of another health problem (NIDDK). The same physiology that this page describes is what a clinician looks at: the NIH says the physical exam often checks for blood vessel, nervous system and hormone issues, and that tests can include blood tests, an ultrasound “to show how blood flows through the penis,” and a nighttime erection test that can help show whether ED is due to a physical problem (NIDDK, Diagnosis of ED). Do not stop or change a prescribed medicine on your own if you suspect it is involved; raise it with the clinician who prescribed it.

The bottom line

An erection starts with nerve signals, runs on nitric oxide and cGMP relaxing smooth muscle, and depends on arteries bringing blood in and compressed veins keeping it there. ED medicines strengthen that natural signal; they do not replace it, which is why they need sexual stimulation. Because nerves, blood vessels, hormones, medicines and mood can all affect the chain, the useful next step when erections change is a clinician’s look at the whole picture.

Sources

Every clinical statement on this page traces to a primary or peer-reviewed source:

• NIH NIDDK, Definition & Facts for Erectile Dysfunction (last reviewed October 2024): about 40% of men affected at age 40 and 70% by age 70; ED is not a routine part of aging.
• NIH NIDDK, Symptoms & Causes of Erectile Dysfunction (last reviewed October 2024): conditions affecting blood vessels, nerves or hormones; nerve disorders including MS, spinal cord injury and pelvic surgery damage; heart and blood vessel diseases; medicines; anxiety, depression and stress; lifestyle factors; ED may be a symptom of another health problem.
• NIH NIDDK, Diagnosis of Erectile Dysfunction (last reviewed October 2024): physical exam for blood vessel, nervous system and hormone issues; blood tests, ultrasound of penile blood flow and the nocturnal erection test.
• VIAGRA (sildenafil citrate) prescribing information, section 12.1 Mechanism of Action, DailyMed: nitric oxide release during sexual stimulation, guanylate cyclase, cGMP and smooth muscle relaxation; PDE5 breaks down cGMP; sildenafil has no direct relaxant effect and no effect without sexual stimulation.
• Dean RC, Lue TF. Physiology of penile erection and pathophysiology of erectile dysfunction (Urol Clin North Am, 2005): arterial dilation, trapping and venous compression; autonomic and somatic nerve roles; brain centers; cavernous nerves and pelvic surgery; calcium and cGMP in smooth muscle relaxation; how erections end; psychogenic, neurogenic, arterial and venous mechanisms of ED; the endothelium.
• Hoppe H, Diehm N. Percutaneous Treatment of Venous Erectile Dysfunction (Front Cardiovasc Med, 2021): definition of venous leak; potential risk factors; how it is confirmed; treatment results reported in a meta-analysis and the need for further studies.