Now, Johns Hopkins scientists say they have reason to believe that the problem is rooted in the failure of cells that line the blood vessels to allow the arteries to expand to accommodate increased blood flow during exertion.
"Our study shows that this impaired ability of the endothelial cells, which control large blood vessel relaxation, is a potential cause of exercise hypertension," says Kerry J. Stewart, Ed.D., lead study author and director of clinical exercise physiology at Hopkins. "Because as many as 90 percent of adults are at risk for developing high blood pressure, knowing this may point to a cellular target for preventive therapies."
Normally during exercise, blood pressure increases to push the flow of oxygen-rich blood throughout the body. However, in some individuals, the response to exercise is exaggerated. Instead of reaching a systolic (upper number) blood pressure of around 200 mmHg at maximal exercise, they spike at 250 mmHg or higher.
For the study, published in the April issue of the American Journal of Hypertension, the investigators evaluated 38 men and 44 women ages 55 to 75 who had untreated mild hypertension but were otherwise healthy. Their blood pressures at rest ranged from 130 to 159 mmHg systolic (the upper number) and 85 to 99 mmHg diastolic (the lower number).
To measure endothelial function, the researchers first used ultrasound to measure the size of a large artery in the arm. Next they put a tight blood pressure cuff on one of the subjects' arms for five minutes to stop blood flow to the arm, then deflated the cuff, causing a surge of blood flow. They then repeated the artery size measurement, comparing it to the resti
Contact: Joanna Downer
Johns Hopkins Medical Institutions