Abstract |
Over the past few years, increasing evidence has supported the possible role of uric acid as a mediator of high blood pressure. Both animal model data and tissue culture experiments suggest that uric acid might cause increased blood pressure through a 2-phase process. The first phase is dominated by a uric acid-mediated vasoconstriction followed by induction of renal afferent arteriolosclerosis and altered pressure natriuresis, leading to sodium-dependent hypertension. We have assessed children with newly diagnosed essential hypertension through cross-sectional studies and clinical trials. Elevated uric acid is closely associated with new-onset essential hypertension in children, and preliminary data suggest that lowering of uric acid can lower blood pressure in some patients. Future studies will be needed to determine whether the mechanisms shown in animal models can be extrapolated to children.
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Authors | Daniel I Feig, Richard J Johnson |
Journal | Journal of renal nutrition : the official journal of the Council on Renal Nutrition of the National Kidney Foundation
(J Ren Nutr)
Vol. 17
Issue 1
Pg. 79-83
(Jan 2007)
ISSN: 1532-8503 [Electronic] United States |
PMID | 17198939
(Publication Type: Journal Article)
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Chemical References |
- Gout Suppressants
- Uric Acid
|
Topics |
- Adolescent
- Animals
- Disease Models, Animal
- Gout Suppressants
(therapeutic use)
- Humans
- Hypertension
(drug therapy, etiology, physiopathology)
- Hyperuricemia
(complications, drug therapy)
- Rats
- Uric Acid
(metabolism)
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