The penis consists primarily of three cylindrical chambers of erectile tissue enclosed within a dense fibrous sheath called the tunica albufera.
Blood reaches the erectile tissue through the internal pudendal artery, which branches into the penile, deep, and dorsal arteries. The deep arteries supply the cavernous spaces directly.
Venous return happens primarily through the subtunica venules, which pierce the tunica albuginea.
Nervous control is supplied by the autonomic nervous system via the cavernous nerves, blending sympathetic and parasympathetic fibers with somatic input from the pudendal nerve.
In the resting state, the penis remains flaccid due to continuous tonic activity of the sympathetic nervous system. Adrenergic fibers release norepinephrine, which binds to alpha-1 adrenergic receptors on the trabecular smooth muscle and arteriolar walls. This maintains contraction, keeping the vascular smooth muscle constricted, limiting arterial inflow, and allowing open venous drainage.
Sexual arousal begins with tactile, visual, or psychological stimuli that trigger signals from the brain to the sacral spinal cord segments S2 through S4. Parasympathetic nerve fibers via the pelvic splanchnic nerves take over, releasing acetylcholine at the nerve terminals within the penis. This action inhibits sympathetic vasoconstriction and initiates the relaxation cascade.
Acetylcholine stimulates endothelial cells to synthesize nitric oxide (NO) via endothelial nitric oxide synthase. NO diffuses into adjacent trabecular smooth muscle cells and activates guanylyl cyclase, which converts GTP into cyclic guanosine monophosphate (cGMP). Accumulation of cGMP decreases intracellular calcium levels, causing smooth muscle relaxation. Phosphodiesterase type 5 (PDE5) breaks down cGMP to end the response.
As cGMP levels rise and intracellular calcium drops, the trabecular smooth muscle relaxes. This relaxation opens up the cavernous sinusoidal spaces, allowing blood to rush in from the dilated helicine arteries. The sinusoidal spaces expand rapidly, accommodating high volumes of blood and causing the penis to elongate and swell.
Full rigidity requires the veno-occlusive mechanism. As the sinusoidal spaces expand, they compress the subtunica venules against the rigid, inelastic tunica albuginea. This compression traps blood inside the corpora cavernosa, drastically reducing venous outflow. Arterial inflow matches this trapped pressure, achieving full penile rigidity.
Following ejaculation or the removal of sexual stimulation, the erection subsides through detumescence. Sympathetic tone returns, releasing norepinephrine which contracts the trabecular smooth muscle. At the same time, phosphodiesterase type 5 breaks down cGMP. The veno-occlusive mechanism reverses as the sinusoidal spaces empty, allowing normal venous outflow and returning the penis to flaccidity.