Abstract |
The association between fructose and increased blood pressure is still incompletely defined, because experimental studies have produced dissimilar conclusions. Amplified vasopressor responses to minimal stimuli and differing responses to fructose in peripheral versus central sites may explain the controversy. Fructose induces systemic hypertension through several mechanisms mainly associated with deleterious effects on target organs (kidney, endothelium, heart) exerted by the byproducts of its metabolism, such as uric acid. The kidney is particularly sensitive to the effects of fructose because high loads of this sugar reach renal tissue. In addition, fructose increases reabsorption of salt and water in the small intestine and kidney; thus the combination of salt and fructose has a synergistic effect in the development of hypertension. Clinical and epidemiologic studies have also linked fructose consumption with hypertension. Further studies are warranted in order to understand the role of fructose in the development of hypertension.
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Authors | Magdalena Madero, Santos E Perez-Pozo, Diana Jalal, Richard J Johnson, Laura G Sánchez-Lozada |
Journal | Current hypertension reports
(Curr Hypertens Rep)
Vol. 13
Issue 1
Pg. 29-35
(Feb 2011)
ISSN: 1534-3111 [Electronic] United States |
PMID | 20957458
(Publication Type: Journal Article, Review)
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Chemical References |
- Sodium Chloride, Dietary
- Sweetening Agents
- Vasopressins
- Uric Acid
- Fructose
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Topics |
- Animals
- Blood Pressure
(drug effects)
- Disease Models, Animal
- Endothelium, Vascular
- Fructose
(administration & dosage, adverse effects, metabolism)
- Humans
- Hypertension
(chemically induced, epidemiology, etiology)
- Kidney Diseases
- Metabolic Syndrome
- Oxidative Stress
- Risk Factors
- Sodium Chloride, Dietary
(administration & dosage, adverse effects, metabolism)
- Sweetening Agents
(administration & dosage, adverse effects, metabolism)
- United States
(epidemiology)
- Uric Acid
(metabolism)
- Vasopressins
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