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Senior Citizen Health & Medicine
Hardening of the Arteries Caused by a Communications
Failure
Old arteries not getting message to relax as
they did when young
 November 6, 2006 – A diagnosis feared by senior
citizens – "hardening of the arteries" – may be caused by a lack of
communications, says new research. The old blood vessels still have the
ability to relax, much as they did when they were younger, but they are
not getting the message. It is this age-related loss of elasticity that
often is a prelude to high blood pressure and cardiovascular disease.
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Health & Medicine |
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Researchers in the Linus Pauling Institute at
Oregon State University say they have discovered a fundamental mechanism
that causes aging blood vessels to lose this critical elasticity.
An understanding of this mechanism, scientists say,
provides an important new target for both drugs and dietary changes that
might help prevent or treat atherosclerosis and heart disease. This is a
leading cause of death around the world that, in some form, affects
about 80 percent of older Americans.
"This could ultimately provide a new, fundamental
and possibly inexpensive way to treat or prevent high blood pressure,"
said Tory Hagen, an OSU associate professor of biochemistry and
biophysics, and lead author on the study.
"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."
The research, which was done in test tubes and
animal models, needs to be confirmed in humans before it could form the
basis for new therapies.
But the fundamental findings reveal an important
insight into how blood vessels change with age and lose much of their
ability to relax, contract, and facilitate the circulation of blood in
the body.
Blood vessels in humans, like those of other
animals, have vascular "smooth muscles" that can alternatively relax and
contract to accommodate fluctuations in blood flow and volume. A thin
layer of "endothelial cells" in the vessels serves, in part, as a sensor
mechanism to help regulate this process. And proper function of the
endothelial cells, in turn, is driven by specific enzymes and signaling
pathways.
What has been known for some time is that blood
vessels, as they age, lose much of their capacity to relax – according
to the OSU research, about half of that capacity, even in healthy
vessels. If the vessels are narrowed by atherosclerotic lesions the
problem is further exacerbated. High blood pressure is often the result,
which in turn can lead to heart attacks, strokes, and death.
Some of the most common high blood pressure
medications, in fact, function by helping to address this loss of
elasticity in blood vessels. The nitroglycerin pills used by many people
with unstable angina provide an immediate boost of nitric oxide, which
serves to relax blood vessels.
What has not been known is exactly why this
"hardening" of the blood vessels occurs with age. The new OSU study
answers much of that question.
"Basically, we've learned that in older blood
vessels, the cellular signaling process is breaking down," said Hagen.
"The vessels still have the ability to relax much
as they did when they were younger, but they are not getting the
message."
A complex enzymatic process outlined in the new
study explains how this "failure to communicate" occurs. An enzymatic
reaction called "phosphorylation," which is essential to the signaling
process, loses about half of its effectiveness in aging blood vessels.
This loss of phosphorylation is due to less activity in one enzyme, AKT,
that facilitates the process, and excess activity of phosphatases, that
reverse it.
The researchers also discovered that ceramides, one
type of lipid, or fat, are primarily responsible for the excessive
activity of phosphatases. And in laboratory experiments with blood
vessels from rats, they were able to inhibit ceramide synthesis.
"The laboratory studies were very compelling,"
Hagen said. "We were able to make aging blood vessels behave as if they
were young again."
According to Balz Frei, professor and director of
the Linus Pauling Institute, and co-author on this study, a strength of
this approach is that it points the way to use diet to prevent the
decline in blood vessel function with age, and to treat it, if
necessary, through drugs.
"A compound we're already using showed the ability
to lower ceramide levels and improve the cell signaling process, and
this compound would be a good starting point for possible drug
therapies," Hagen said. "And certain types of diet may help reduce this
natural, age-related process."
As is appropriate for many other disease concerns
and health conditions, Frei said, a diet that's heavy in fruits and
vegetables seems to slow down the loss of blood vessel function.
However, the scientists also are doing research with lipoic acid, a
powerful antioxidant, that is very promising and may ultimately show it
could play a role as a dietary supplement to help address this problem.
This overall process, the researchers said, is
linked to a low-grade, chronic inflammation that occurs with aging, in
blood vessels and probably many other metabolic functions. Efforts to
understand and address these inflammatory processes are some of the most
promising areas of chronic disease prevention and treatment, they said.
The findings were just published in Aging Cell, a
professional journal. The study was funded by the National Institute on
Aging, National Center for Complementary and Alternative Medicine, and
the American Heart Association.
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