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(Hypertension. 2008;51:8.)
© 2008 American Heart Association, Inc.
Brief Reviews |
From the Department of Cell Biology (Z.V.W.), Albert Einstein College of Medicine, Bronx, NY; and the Touchstone Diabetes Center (Z.V.W., P.E.S.), Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas.
Correspondence to Philipp E. Scherer, Touchstone Diabetes Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-8549. E-mail Philipp.Scherer@utsouthwestern.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
|---|
1.5 billion people, on the globe in the next 20 years.2 Mechanistically, endothelial dysfunction, increased renin-angiotensin system (RAS) activity, and sympathetic nervous system (SNS) hyperactivation have been considered as important risk factors of hypertension and hint at important events taking place at the interface of the endothelium, kidney, and SNS.
Obesity is a global epidemic in children and adults. In the United States, a steady increase of the prevalence of obesity has been found in all states.4,5 It is estimated that 65% of the population is overweight, which is judged by body mass index of 25.0 to 29.9, and 30% are obese (body mass index of
30.0).6 These numbers have been continuously rising in the past 15 years.7 The National Health and Nutrition Examination Survey III for
18 000 adults found that body mass index is an associated risk factor for hypertension independent of age, sex, race, and smoking.8 A long-term weight/hypertension relationship
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