The human penis is composed of the paired dorsal corpora cavernosa and the ventral corpus spongiosum each of which is encased within a fibrous sheath, the tunica albuginea, and then all of which are enclosed within Buck’s fascia, Colles’ fascia, and the skin.

The spongiosum contains the urethra and is contiguous with the glans distally. The arterial supply to the penis is from the four terminal branches of the paired penile arteries, which are themselves branches of the internal pudendal arteries. The external iliac, obturator, vesical, and femoral arteries provide accessory arterial supply to the penile artery in some cases.

Venous outflow originates from postcavernous venules that coalesce to form emissary veins. These veins empty into the cavernous vein, the deep dorsal vein, and the superficial dorsal vein depending on their origin within the penis. Efferent innervation is from parasympathetic, sympathetic, and somatic sources. Somatosensory afferents course from the penis to central sites.

The maintenance of penile flaccidity and the erectile response are controlled via intercommunicating supraspinal and spinal reflex pathways. During the flaccid state, antierectile neural input, primarily via sympathetic efferents, acts to limit blood flow to the penis to a quantity sufficient to meet physiologic needs but insufficient for erection. Following either physical or psychological sexual stimulation proerectile neural signals are sent to the penis primarily via parasympathetic tracts. This input initiates the erectile response via neurotransmitter release onto postsynaptic smooth muscle cells within the corporal bodies.

Nitric Oxide (NO) is the main proerectile neurotransmitter. The resultant molecular cascade leads to a decrease in intracellular Ca2+ and arteriolar smooth muscle relaxation.

This relaxation allows for increased blood flow and subsequent corporal engorgement with increasing penile rigidity. As the corpora become engorged, the emissary veins are compressed by within the tunica albuginea limiting venous outflow.

The increased arterial inflow and limited venous outflow increases intracorporal pressure and leads to erection. As proerectile input ceases, the secondary molecular messenger cGMP is hydrolyzed allowing for a rise intracellular Ca2+, subsequent smooth muscle contraction, decreased penile blood flow and a return to flaccid state physiology.