New Insight into Urate-Related Mechanism of Cardiovascular Damage
Davide Grassi, Giovambattista Desideri and Claudio Ferri
Affiliation: University of L'Aquila, Department of Life, Health, and Environmental Sciences, Viale S Salvatore, Delta, 6 Medicina, 67100 Coppito, L'Aquila, Italy.
Keywords: Uric acid, hyperuricemia, endothelial dysfunction, oxidative stress, cardiovascular risk.
Several experimental and clinical studies reported that hyperuricemia may trigger hypertension, metabolic syndrome, vascular
damage and renal disease. Furthermore, a substantial proportion of epidemiological studies are compatible with the hypothesis that hyperuricemia
may be an indipendent risk factor for cardiovascular disease as well as for an increased cardiovascular mortality. Xanthine
oxidase is a critical source of reactive oxygen species contributing to vascular inflammation and endothelial dysfunction. Although a
causal relationship between these conditions has not been clearly clarified, the capacity of uric acid to negatively affect vascular function
by pro-oxidant effects and by decreasing nitric oxide bioavailability and consequently induce endothelial dysfunction may explain the association
among hyperuricemia, hypertension, metabolic syndrome, and cardiovascular disease, also by a common mechanicistic point of
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