A team of Hopkins scientists has greatly advanced the science of penile erection, showing for the first time the mechanism for continued production of nitric oxide that maintains an erection over time. The findings are published in the March 19 issue of the Proceedings of the National Academy of Sciences.
"The physiology of erection is like driving a car," says Arthur Burnett, M.D., associate professor of urology at Hopkins and senior author of the study. "You can't just turn the key and expect to go anywhere. You also need to hit and hold the accelerator."
Researchers at Hopkins ten years ago discovered that release of nitric oxide from nerve endings in the penis caused erection, but the temporary release of nitric oxide – a neurotransmitter that survives just a few seconds before breaking down – couldn't explain how erections are naturally sustained over time.
Working with rats and genetically transformed mice, Hopkins scientists found that after an initial burst of nitric oxide from nerve endings triggers erection, blood vessels release more nitric oxide to harden and maintain the erection.
"Once blood starts flowing into the penis, the source of nitric oxide in the blood vessels is continuously activated so that more nitric oxide is released, more tissue relaxes, more blood comes in and a sustained erection is achieved," Burnett says.
This cascade of events, Burnett says, begins when erotic thoughts or physical sensations produce nitric oxide release in nerve endings in the penis. Nitric oxide is a relaxant that allows blood vessels to open up or dilate, bringing increased blood flow and swelling of tissues. The flow of blood also creates a minor stress on the blood vessel wall which activates the release of more nitric oxide. This time it is from cells in the wall of the blood vessel – the endothelial cells – rather than from nerves. Endothelial nitric oxide causes more tissue to relax and the process repeats until the penis is fully erect.
A key element in the attainment of erection is the continuous activation of the source of nitric oxide in blood vessel walls, according to Burnett. Finding this source, a special form of the enzyme called endothelial nitric oxide synthase (eNOS), plus the discovery that the pressure of flowing blood against a vessel wall could induce it to produce nitric oxide, were critical pieces of the puzzle. These discoveries offer a fuller picture of the complex physiology of erection.
In addition to its application towards new and improved therapies for erectile dysfunction, Burnett says, this understanding of nitric oxide's effect can be extended to other areas of the body that are more difficult to observe, such as the heart and other internal organs.
The research was funded by the U.S. Public Health Service.
Other authors of the study are K. Joseph Hurt, Biljana Musicki, Michael Palese, Julie Crone, Robyn Becker, John Moriarty and Solomon Snyder.
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Journal
Proceedings of the National Academy of Sciences