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Biology Articles » Genetics » Hold The Salt: Gene May Explain African Americans' Extra Sensitivity To Salt, Leading To High Blood Pressure

Hold The Salt: Gene May Explain African Americans' Extra Sensitivity To Salt, Leading To High Blood Pressure

Hold The Salt: Gene May Explain African Americans' Extra Sensitivity To Salt, Leading To High Blood Pressure

ORLANDO, Fla., March 24 -- Having a particular gene may make African Americans much more sensitive to salt, thereby increasing their risk of developing high blood pressure, according to a new report presented here today at the American Heart Association's epidemiology and prevention meeting.

Researchers say they have found that one variant of the angiotensin converting enzyme (ACE) gene can greatly influence an African American's susceptibility to salt, which is called salt-sensitivity. As little as one extra gram of salt, the amount in half a teaspoon of table salt or the 1,000 milligrams in one serving of some processed foods could raise blood pressure as much as five millimeters of mercury (mm Hg) in people who have the gene variant.

"This is a new finding -- no one has reported this association in African Americans," says the study's lead author, John M. Flack, M.D., professor and associate chairman, department of internal medicine, and director of the cardiovascular epidemiology and clinical applications program at Wayne State University in Detroit. African Americans are at greater risk of developing high blood pressure than the general population.

The body produces angiotensin to restrict blood vessels and help regulate blood pressure. The ACE gene controls the amount of angiotensin released into the body. If the ACE gene is flawed, it can cause the blood vessels to constrict too much, raising the pressure of blood flow on blood vessel walls and, consequently, increasing the risk of high blood pressure.

The researchers examined the influence of the ACE gene variant on blood pressure response to sodium intake in 81 African-American men and women who had normal blood pressure readings (less than 140/90 mm Hg). They found that the systolic blood pressure -- the upper number on a blood pressure reading -- rose sharply in those who consumed sodium and had the ACE gene variant when compared to those who did not have the variant.

The association between sodium intake and high blood pressure has been greatly debated. While Flack agrees that not everyone's blood pressure may be affected by sodium intake, he adds that this specific group of salt-sensitive African Americans needs special attention.

"People criticize the concept of reducing sodium because not everyone's blood pressure goes up," says Flack. "While everyone may not need to restrict sodium intake in the short term, buried within that group of people is a subset of people who are really salt-sensitive."

The exact cause of high blood pressure is not completely understood, says Flack. It has been well documented that when exposed to usual and customary levels of dietary salt intake, blood pressure rises in some people considered to be salt-sensitive.

"High blood pressure damages the kidneys, brain, heart, and other vital organs," says Flack. "The rise in blood pressure causes the kidneys to leak protein and also contributes to an abnormal increase in heart size."

Flack says that salt-sensitivity has been documented in all racial and ethnic groups, and even in people with normal blood pressure levels, but he adds that heredity is an important influence on whether an individual is salt-sensitive or not.

"This study is consistent with findings in Japanese and Spanish populations," says Flack. "We're not quite ready to recommend widespread screening for the ACE gene, but we may be getting close to the point where it might be a reasonable thing to do."

Currently, mass screening for the gene variant is not recommended. However, Flack says African Americans who have high blood pressure, diabetes, kidney disease or who are obese have been found to be most likely to have the ACE gene variant.

Co-authors are Beth A. Staffileno, D.N.Sc., Marwan Hamaty, M.D., Amanda Dudley, B.S., Gerard Tromp, Ph.D., and Helena Kuivaniemi, M.D., Ph.D., of Wayne State University; Carla Yunis, M.D., of Wake Forest School of Medicine, Winston Salem, N.C.; and Richard H. Grimm, M.D., Ph.D., of Hennepin County Medical Center, Minneapolis.

The research was presented at the American Heart Association 39th Annual Conference on Cardiovascular Disease Epidemiology and Prevention.

Source: American Heart Association, March 1999


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