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Does a new hypothesis help explain higher levels of hypertension among African-Americans?

(Atlanta, GA) Some 50 million Americans have high blood pressure, according to the American Heart Association, yet the prevalence of essential hypertension -- high blood pressure with no identifiable cause -- is much higher in African-Americans than in Caucasians. While this disparity is well documented, the mechanisms by which stress might contribute to these differences are far less clear.

Most studies have used a "reactivity hypothesis" to help identify the reasons behind the differences. This hypothesis assumes that blacks exhibit exaggerated blood pressure (BP) responses to stress which produce vascular damage that underlies the premature development of essential hypertension. An alternative to this widely accepted approach is the "pressure natriuresis" hypothesis. It supposes that stress-induced impaired sodium (salt) regulation leads to an extended period of elevated BP in blacks, and that the resulting increase in BP load leads to the early development of hypertension and its consequences.

A New Study

The latter approach has been put to the test by a team of researchers. The authors of a new study entitled "Race Differences in Stress-Induced Salt Sensitivity and Resulting Blood Pressure Load," are Gregory A. Harshfield, Martha E. Wilson, Kathryn McLeod, Coral Hanevold, Gaston Kapuka, Lynne Mackey, Lesley Edmunds and Delores Gillis, all of the Medical College of Georgia, Augusta, GA. They will present their findings during the upcoming scientific conference, Understanding Renal and Cardiovascular Function Through Physiological Genomics, a meeting of the American Physiological Society (APS) (www.the-aps.org), being held October 1-4, 2003 at the Radisson Riverfront Hotel and Convention Center, Augusta, GA.

Methodology

To test the hypothesis that stress is a contributing factor through its effects on pressure natriuresis (the excretion of sodium in urine, usually in exce
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Contact: Donna Krupa
djkrupa1@aol.com
703-527-7357
American Physiological Society
30-Sep-2003


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