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ACE Gene Linked To High Blood Pressure In Men But Not Women

DALLAS, May 12 -- Researchers have zeroed in on a gene linked to high blood pressure -- a disease that affects one in four adults -- according to two reports in today's Circulation: Journal of the American Heart Association. Two separate studies found that a variation in a gene called ACE (angiotensin converting enzyme) may be an important contributor to high blood pressure in men. Untreated high blood pressure can lead to heart disease, stroke and kidney failure. The cause of the most common form of high blood pressure, essential hypertension, is unknown.

The researchers from the Framingham Heart Study and the Genetics of Atherosclerosis Network (GENOA), which is part of the Family Blood Pressure Program, used the technique of genetic linkage to track a marker -- a gene that has already been identified within the family and is located on the same chromosome as the "ACE" gene. Researchers then tracked the variants of the gene to see which ones "hold hands" with the marker. Gene variants that travel from one generation to the next and associate with high blood pressure are likely candidates for the high blood pressure gene.

According to Christopher O'Donnell, M.D., lead author of the Framingham Heart Study report, linkage analysis is a powerful tool for scientists to identify a gene region, called a locus, that is involved in specific disease. However, the studies cannot distinguish whether the ACE variant or another gene that is also closely linked to ACE is responsible for raising blood pressure.

"If you think about a person's entire genetic make-up in terms of a large city, we have narrowed the location down to one city block," he says. "However, we are still not sure if we have the right address."

The gene region must now be analyzed for "finer mapping" to reveal the exact "address." Once it is located, scientists can study the ACE variant (or a gene next to it) and det
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Contact: Carole Bullock
caroleb@amhrt.org
214-706-1279
American Heart Association
11-May-1998


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