Daniel I Feig, Duk-Hee Kang, Takahiko Nakagawa, Marilda Mazzali, Richard J Johnson
Author Information
Daniel I Feig: Department of Pediatrics, Renal Section, MC3-2482, Baylor College of Medicine, 1102 Bates Street, Houston, TX 77030, USA. dfeig@bcm.tmc.edu
Epidemiologic studies published during the past 3 years support the possible role of uric acid in the onset of essential hypertension. Data from several large, longitudinal cardiovascular disease studies indicate that elevated serum uric acid is a predictor of incident hypertension and blood pressure progression. In a pediatric study, more than 90% of children with essential hypertension have serum uric acid levels above 5.5 mg/dL. During the same period, laboratory studies have provided compelling mechanistic evidence to explain the clinical observations. Uric acid causes hypertension in a rat model through the activation of the renin-angiotensin system, downregulation of nitric oxide, and induction of endothelial dysfunction and vascular smooth muscle proliferation. Ongoing clinical trials will elucidate the role of uric acid in human hypertension and will determine whether control of uric acid may be a new way to prevent or treat essential hypertension.
