Erection Of The Penis

How does a man get an erection? What is the process behind a penis going from flaccid to erect? Why is a penis normally in the flaccid state? And what is it that causes the erection to end? This page will answer all those questions, and also explain how the penis is built up and which parts of the penis are most important in this erection process.

A Brief Anatomy Of The Penis

There are three main erectile structures inside a human penis: the corpus spongiosum and the two corpora cavernosa. These three structures lay parallel to each other. The corpus spongiosum runs along the bottom of the penis from the base, all the way to the glans, or to the head of the penis. The urethra, which is the tube that carries urine as well as sperm, runs inside the corpus spongiosum. Although the corpus spongiosum does fill with blood during an erection, the overall blood pressure is low and as a result, the corpus spongiosum does not give much support to the erection. This pressure is low in order to allow sperm to pass through the urethra during ejaculation. The parts of the penis that are responsible for making the penis hard are the corpora cavernosa.

The two corpora cavernosa are chambers consisting of networks of open spaces, sinusoids, smooth muscle, nerves and small arteries. Together, these are called the spongy erectile tissue.


During an erection, these two chambers fill with blood and provide the stiffness of the erection. Another key part that supports the erection is the layer around the corpora cavernosa called the tunica albuginea. This layer or membrane is of limited flexibility. Therefore, when blood flows into the penis, the tunica albuginea ensures pressure builds up inside the corpora cavernosa. As a result, the corpora cavernosa become firm and the penis as a whole becomes erect.

This can simplistically be compared to filling a bike tire with air: as the inner tube becomes filled with air, pressure increases, the outer rubber provides resistance and the tire becomes firm and hard. Also, the wall between the two units of corpora cavernosa has a number of openings that let blood flow freely between the two sides so that the pressure is similar in both of these chambers. As the tunica albuginea expands outward, it also squeezes off the drainage veins at the bottom of the corpora cavernosa, which traps the blood and increases the blood pressure inside the penis.

There are three main arteries that supply blood to the penis: the cavernosal artery, the dorsal artery, and the bulbourethral artery. All three arise from an internal artery called the penile artery.

The corpus spongiosum, the two corpora cavernosa, and the tunica albuginea are surrounded by something called the Buck’s fascia. The Buck’s fascia is a strong, deep, fascial layer that sits on top of the tunica albuginea, and this is in turn surrounded by the penile skin which we see externally.

The Process Of A Penis Erection 

Leonardo Da Vinci, through his dissection of human bodies, was the first scientist to realize that during an erection, the penis fills with blood. During his investigation, Da Vinci wrote, “The penis does not obey the order of its master, who tries to erect or shrink it at will, whereas instead the penis erects freely while its master is asleep. The penis must be said to have its own mind, by any stretch of the imagination.”

The reason a penis is normally kept in a flaccid state, is because the smooth muscles inside the erectile structures of the penis are contracted. These contracted muscles keep the tiny arteries inside the erectile tissue squeezed shut, allowing only tiny amounts of blood to flow into the penis to keep up penis maintenance and to provide nutrients and other essential components.

This minimal bloodflow keeps blood pressure inside the corpora cavernosa space low ‚Äď lower than the average blood pressure in¬†arteries¬†throughout the rest of the body. And as long as this blood pressure is adequately low, blood will not flow into the penis and the penis will remain flaccid.

This changes when a man gets ‘turned on’. Dopamine then sets off a chain reaction that starts the process of making the penis erect. Levels of¬†calcium, the chemical whose job it is to keep the smooth muscles contracted, are decreased. The smooth muscles then relax and open up, and blood is allowed to flood into the penis. As blood enters the corpora cavernosa, these chambers starts getting filled up, blood is pushing on the tunica albuginea, and firmness and pressure is building.


This was the easy explanation of how an erection works. The more complicated and detailed process behind a penis erection is described below.

The process of a penis to become erect is normally started when a man has a sexual thought or experiences some form of sexual stimulation. This stimulation could for instance be a kiss or a touch. This in turn, releases dopamine in the brain and sets off signals that are sent from the brain through special autonomic nerves to the spinal cord and the cavernous nerves that run along the prostate gland to reach the corpora cavernosa, the corpus spongiosum and the arteries that supply them with blood.

In the penile flaccid state, the smooth muscles of the corpora cavernosa and the corpus spongiosum are contracted, allowing only a small amount of bloodflow to these parts of the penis for nutritional and maintenance purposes. This flaccid state is achieved by a high concentration of free calcium in the smooth muscles of the penis. This free calcium keeps the smooth muscles is in a state of contraction, and unless the free calcium is reduced, the penis will remain flaccid.

After the signals from the brain have arrived, a process is started that gets the enzyme nitric oxide synthase activated. This enzyme acts as a catalyst for the endothelial cells to manufacture nitric oxide from l-argenine and oxygen, and then diffuses this nitric oxide into the smooth muscles in the corpora cavernosa and the corpus spongiosum. Nitric oxide then binds to a molecule called guanylyl cyclase. To learn more about nitric oxide on Truelibido, please go here.

This in turn converts a¬†molecule¬†in the blood called guanosine trisphosphate to a chemical called cyclic guanosine monophosphate (‘cGMP’). cGMP is a key component in the¬†erection¬†process as it decreases free calcium concentrations.¬†cGMP¬†also helps¬†deactivate¬†the¬†calcium¬†sensitizing mechanism in the penis as receptors connected to proteins that help drive the contraction of¬†smooth muscle¬†cells decrease sensitivity to free calcium.

This reduction of free calcium induces relaxation of the cavernosal smooth muscle cells. As these smooth muscles relax, blood starts to freely flow into the corpora cavernosa and the corpus spongiosum, and the erection is starting to build.

The increased bloodflow expands the corpora cavernosa which then stretches the tunica albuginea (the membrane of limited elasticity on the outside of the corpora cavernosa). As the tunica albuginea stretches, it builds up pressure and firmness. This pressure also compresses the veins at the bottom of the penis where blood would normally flow out of the penis. Or put differently, the pressure makes the tunica albuginea block off the veins that take blood away from the corpora cavernosa. This traps blood within the penis, the pressure increases and the penis becomes erect.

The continuation of the erection is made possible by the tunica albuginea which acts as a gatekeeper by keeping up the pressure and pressing down on the veins that hold blood off from flowing out of the penis.


Testosterone is another key ingredient in the erection process. Nitric oxide synthase is highly dependent on testosterone to function properly, and if there is an inadequate level of testosterone, this will normally cause these enzymes to produce less than optimal amounts of nitric oxide. The reason for this is that lower than normal levels of testosterone will normally cause a decrease in the number of nitric oxide synthase neurons in the brain. To learn more about testosterone on Truelibido, please go here.

Additionally, a certain level of testosterone needs to be present in order for dopamine to be released (or synthesized) as testosterone is one of the ingredients needed for this dopamine creation. And also, increased nitric oxide production in turn causes further dopamine release. To learn more about dopamine on Truelibido, please go here.

When a man has had an orgasm, or sexual stimulation is ceased, the erection will normally fade. The mechanism behind the end of an erection is the reverse of the process of the erection taking place. The amounts of cGMP in the penis are decreased and therefore, levels of free calcium are allowed to increase. When free calcium levels are increased, the smooth muscles in the penis will again contract. Blood is then forced out of the penis by the contracting tissues, and the erection ends.

In short, both contraction and relaxation of the smooth muscles in the erectile structures of the penis are regulated by free calcium, therefore free calcium also regulates the onset and end of a man’s¬†erections.

There are pharmaceutical drugs that target this free calcium level in order to help a man both get an¬†erection¬†and also maintain the¬†erection¬†for longer than would otherwise be possible. Viagra, Cialis and Levitra¬†all do this. These drugs act on an enzyme called phosphodiesterase type 5 (‘PDE5’). This enzyme is part of the¬†erection¬†process as it helps control the level of cGMP, or rather, it breaks down cGMP. When cGMP is broken down, the free calcium levels are allowed to rise, smooth muscles start to contract and blood will flow out of the penis. What these drugs do is to inhibit this PDE5 so that it does not break down cGMP (or breaks it down much slower). When there is more cGMP present, this will decrease free calcium¬†levels and the¬†erection¬†builds and is allowed to remain.

Research Studies

Aboseif SR, Lue TF. Fundamentals and hemodynamics of penile erection. CardioVascular and Interventional Radiology, 1988, Volume 11, Issue 4, pp 185-190.

Andersson KE. Mechanisms of Penile Erection and Basis for Pharmacological Treatment of Erectile Dysfunction. Pharmacol Rev. 2011.

Andersson KE. Pharmacology of penile erection. Pharmacol Rev. 2001; 53: 417-50.

Andersson, KE Wagner G. Physiology of penile erection. Physiological Reviews Published 1 January 1995 Vol. 75 no. 1, 191-236.


Argiolas A, Melis MR. Neuromodulation of penile erection: an overview of the role of neurotransmitters and neuropeptides. Progress in Neurobiology, Volume 47, Issues 4‚Äď5, November‚ÄďDecember 1995, Pages 235‚Äď255.

Benson G, McConnell J, Lipschults L. Neuromorphology and neuropharmacology of the human penis. J. Clin. Invest. 1980; 65:506.

Borowitz E, Barnea O. Hemodynamic mechanisms of penile erection. IEEE Trans Biomed Eng. 2000 Mar; 47(3):319-26.

Breza J, Aboseif S, Orvis B. Detailed anatomy of penile neurovascular structures: surgical significance. J. Urol. 1989; 141:437.

Christianson DW. Arginase: structure, mechanism, and physiological role in male and female sexual arousal. Acc Chem Res. 2005;38: 191-201.

Conti G, Virag R. Human penile erection and organic impotence: Normal histology and histopathology. Urol. Int. 1989; 44:303.

Creed KE, Carati CJ, Keogh EJ. The physiology of penile erection. Oxford Reviews of Reproductive Biology, 13. pp. 73-95.

Dean RC, Lue TF. Physiology of penile erection and pathophysiology of erectile dysfunction. Urol Clin North Am. 2005;32: 379-95.

Lue TF, Tanagho EA. Physiology of erection and pharmacological management of impotence. J Urol. 1987;137: 829-36.

Nehra A, Goldstein I, Nugent M, Huang Y, de las Morenas A, Krane R, Udelson D, de Tejada I, Moreland R. Mechanisms of venous leakage: a prospective clinicopathologic correlation of corporal structure and function. J. Urol. 1996; 156:1320‚Äď1329.

Newman HF, Northup JD. Mechanism of human penile erection: an overview. Urology. 1981 May; 17(5):399-408.

Nunes KP, Webb RC. Mechanisms in Erectile Function and Dysfunction: An Overview. ISBN: 978-953-51-0199-4; DOI: 10.5772/39088.

S√°enz de Tejada I, Angulo J, Cellek S, Gonz√°lez-Cadavid N, Heaton J, Pickard R, Simonsen U. Physiology of erectile function. J Sex Med. 2004; 1: 254-65.

Sullivan ME , Thompson CS, Dashwood MR, Khan MA, Jeremy JY, Morgan RJ, Mikhailidis DP. Nitric oxide and penile erection: Is erectile dysfunction another manifestation of vascular disease? Cardiovascular Research 43, (1999) 658‚Äď665.

Toda N, Ayajiki K, Okamura T. Nitric oxide and penile erectile function. Pharmacol Ther. 2005;106: 233-66.

Traish AM. Biochemical and Physiological Mechanisms of Penile Erection. Sexuality and Disability, June 2004, Volume 22, Issue 2, pp 151-160.


Udelson D, Nehra A, Hatzichristou D, Azadzoi K, Moreland R, Krane R, Saenz de Tejada I, Goldstein I. Engineering analysis of penile hemodynamic and structural‚Äďdynamic relationships: part I‚ÄĒclinical implications of penile tissue mechanical properties. Int. J. Impot. Res. 1998a; 10:15‚Äď24. DOI: 10.1038/sj.ijir.3900310.

Udelson D, Nehra A, Hatzichristou D, Azadzoi K, Moreland R, Krane R, Saenz de Tejada I, Goldstein I. Engineering analysis of penile hemodynamic and structural‚Äďdynamic relationships: part II‚ÄĒclinical implications of penile buckling. Int. J. Impot. Res. 1998b; 10:25‚Äď35. DOI:10.1038/sj.ijir.3900311.

Udelson D. Biomechanics of male erectile function. J R Soc Interface. 2007 Dec 22; 4(17): 1031‚Äď1048.

Wespes E, Schulman C. Parameters of erection. Br. J. Urol. 1984; 56:416‚Äď417.

Yiee JH, Baskin LS. Penile embryology and anatomy. ScientificWorldJournal. 2010; 10: 1174-9.

Zavara P, Sioufi R, Schipper H, Begin L, Brock G. Nitric oxide mediated erectile activity is a testosterone dependent event: a rat erection model. Int. J. Impot. Res. 1995; 7:209‚Äď219.

Comments Off on Erection

Comments are closed.

Social media & sharing icons powered by UltimatelySocial