Lack of Potassium Linked to High Blood Pressure

The finding is especially true for blacks, study suggests

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SUNDAY, Nov. 9, 2008 (HealthDay News) -- Consuming too little potassium may be as big a risk factor for high blood pressure as eating too much sodium, especially for blacks, new research says.

The study also identified a gene that may influence potassium's effects on blood pressure.

The findings, based on a Texas heart study done on the urine samples of 3,300 people, support previous studies that made similar conclusions about potassium and blood pressure.

The new study was to be presented Saturday at the American Society of Nephrology's annual meeting, in Philadelphia.

"The lower the potassium in the urine, hence the lower the potassium in the diet, the higher the blood pressure," lead study author Dr. Susan Hedayati, of the University of Texas Southwestern Medical Center at Dallas, said in a news release issued by the conference organizers. "This effect was even stronger than the effect of sodium on blood pressure."

The link between high blood pressure and low potassium was strong even when age, race, and other cardiovascular risk factors, such as high cholesterol, diabetes and smoking, were factored in. About half the study participants were black, and they tended to consume the least amount of potassium in their diet, Hedayati said.

Laboratory research for the study suggests that the WNK1 gene may be responsible for potassium's effects on blood pressure. More research is being done to test how fixed levels of potassium in a diet affect blood pressure and the gene's activity.

Meanwhile, the researchers urged people to consume more potassium and less sodium. "High-potassium foods include fruits such as bananas, and citrus fruits and vegetables," Hedayati said. "Consuming a larger amount of these foods in the diet may lower blood pressure."

More information

The American Academy of Family Physicians has more about lowering your blood pressure.

SOURCE: American Society of Nephrology, news release, Nov. 8, 2008

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