Researchers at the Linus Pauling Institute at Oregon State University (OSU) report that they have discovered a new mechanism that causes aging blood vessels to lose their elasticity. “This could ultimately provide a new, fundamental, and possibly inexpensive way to treat or prevent high blood pressure,” says Tory Hagen, associate professor of biochemistry and biophysics at OSU and lead author of the study.
Until now, researchers didn’t know why the arteriosclerosis occurred with age. “It’s also a key to understanding the biological effects of inflammation, which increasingly seems to be implicated not only in heart disease but other chronic and neurologic diseases,” adds Hagen.
The research, which was done in vitro and in animal models, needs to be confirmed in humans before it can form the basis for new therapies. However, the fundamental findings reveal how blood vessels change with age and lose much of their ability to relax, contract, and facilitate the circulation of blood in the body. “Basically, we’ve learned that in older blood vessels the cellular signaling process is breaking down,” says Hagen. “The vessels still have the ability to relax as they did when they were younger but they are not getting the message.”
The study published in Aging Cell identifies phosphorylation as a player in this failure to communicate. Phosphorylation loses about half of its effectiveness in aging blood vessels due to lowered activity in AKT.
Ceramides are primarily responsible for inhibiting the activity of AKT. However, in laboratory experiments with blood vessels from rats, the researchers were able to inhibit ceramide synthesis. This made the aging blood vessels behave like young blood vessels.
“A compound we’re already using showed the ability to lower ceramide levels and improve the cell signaling process. This compound would be a good starting point for possible drug therapies,” says Hagen. “Certain types of diet may also help reduce this natural, age-related process.”