Changes in blood vessel chemistry may explain why estrogen changes
from a heart protector to a heart danger as women age. Before menopause,
estrogen functions as a dilator of blood vessels, offering a protective
effect to the heart. However, later in life estrogen's function
changes to a constrictor of blood vessels, which could be dangerous.
Researchers hope their further understanding of estrogen's role
in the body will help to make hormone replacement therapy (HRT)
safer. A 15-year study of more than 161,000 women found that HRT,
though promoted to reduce the risk of heart attack and stroke in
postmenopausal women, actually increases the risk. Doctors were
left puzzled at the conflicting findings.
Researchers began studying the effect of estrogen on blood vessels
and found that estrogen targets the enzyme nitric oxide synthase
1, which makes the vasodilator, nitric oxide. They tried to block
estrogen's activity by blocking nitric oxide, and found that, surprisingly,
the estrogen had changed into a constrictor agent, one that would
increase blood pressure.
Further, it was found that aging naturally decreases levels of
the cofactors L-arginine and tetrahydrobiopterin, which are both
necessary to nitric oxide synthase's production of nitric oxide.
Rather than making nitric oxide, the estrogen was making an age-promoting
and vasoconstricting oxygen free radical, superoxide.
Superoxide is an oxidant that causes cellular damage and, researchers
found, constriction. They noted that estrogen is a powerful agent--one
that can affect every bodily system. As cofactors drop that enable
estrogen to relax blood vessels, the researchers question what effects
it will have on blood pressure, Alzheimer's and other systems in
the body.
Medical
College of Georgia February 16, 2005
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