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During sexual arousal, the penis becomes erect, enabling penetration during sexual intercourse. An erection results from a complex interaction of neurologic, vascular, hormonal, and psychologic stimuli. Pleasurable stimuli cause the brain to send nerve signals through the spinal cord to the penis. The arteries supplying blood to the corpora cavernosa and corpus spongiosum respond by widening (dilating). The widened arteries dramatically increase blood flow to these erectile areas. At the same time, muscles around the veins that normally drain blood from the penis tighten, slowing the outflow of blood and elevating blood pressure the penis. This combination of increased inflow and decreased outflow is what causes the penis to become engorged with blood and increase in length, diameter, and stiffness.
At the climax of sexual excitement (orgasm), ejaculation usually occurs, caused when stimulation of the glans penis and other stimuli send signals to the brain and spinal cord. Nerves stimulate muscle contractions along the seminal vesicles, prostate, and the ducts of the epididymis and vas deferens. These contractions force semen into the urethra. Contraction of the muscles around the urethra further propels the semen through and out of the penis. The neck (base) of the bladder also constricts to keep semen from flowing backward into the bladder.
Once ejaculation takes place—or the stimulation stops—the arteries constrict and the veins open, reducing blood inflow, increasing blood outflow, and causing the penis to become limp (detumescence). After detumescence, erection cannot be obtained for a period of time (refractory period), commonly about 20 minutes in young men.
Last full review/revision February 2013 by Irvin H. Hirsch, MD
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