Like the poles and ropes that support a circus tent, something has to keep an erect penis up. But until now, that something has been a mystery. A new study shows that an enzyme in the cells that line the blood vessels of the penis maintains erections by pumping out nitric oxide (NO). The finding fleshes out NO's role in sexual arousal and could pave the way to new treatments for sexual dysfunction in men, and possibly women.
Almost a decade ago, researchers identified NO as the small molecule that triggers erections. Sexual stimulation spurs nerves in the penis to release NO, which tells normally condensed smooth muscle in the penis to loosen up. Blood rushes into and expands the spongy tissue surrounded by the muscle like air rushing into a balloon. How the erection is sustained, however, was anyone's guess.
Researchers led by uroneurologist Arthur Burnett of Johns Hopkins University in Baltimore, Maryland, suspected that NO played an ongoing role. They took a closer look at an NO-producing enzyme called NO-synthase (NOS) found in the endothelial cells lining penile blood vessels and spongy tissue. In experiments with rats, 15 seconds of mild electrical stimulation of the penis boosted the amount of active NOS by 40%, the team reports in the 19 March issue of the Proceedings of the National Academy of Sciences. Chemicals that prevented NOS activation reduced the blood pressure inside stimulated penises--indicating the enzyme was needed to maintain an erection. The NOS produced by nerve cells, on the other hand, didn't seem to play a role in maintenance: Whereas engineered mice lacking the endothelial NOS failed to maintain erections, mice lacking only the neuronal NOS had no such problems. The researchers suggest that the neuronal NOS initiates erections, then the endothelial NOS kicks in to keep the party going.
These results could help treat sexual dysfunction in both men and women, says Burnett, because female genitals also contain the endothelial NO-synthase. Urologist Tom Lue of the University of California, San Francisco, says that the work opens up new avenues of research. "A lot of diseases affect endothelial cells," he says. Conditions such as high cholesterol might interfere with the NO-synthase, he suggests, and thereby contribute to male impotence.