Hyperuricemia, endothelial dysfunction and hypertension

The final product of purine bases degradation in humans, reptiles and other primates is uric acid. The serum level of uric acid can be influenced by diet, certain systemic pathologies and a decreased renal excretion. Xanthine oxidase (XO) catalyzes the formation of uric acid with generation of react...

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Published inPractica medicală (2006) Vol. 15; no. 2; pp. 178 - 182
Main Authors Miricescu, Daniela, Totan, Alexandra, Stefani, Constantin, Stanescu, Iulia-Ioana, Imre, Marina, Stanescu, Ana Maria Alexandra, Radulescu, Radu, Balan, Daniela, Balcangiu-Stroescu, Andra-Elena, Greabu, Maria
Format Journal Article
LanguageEnglish
Published Amaltea Medical Publishing House 30.06.2020
Subjects
endothelial dysfunction
hypertension
hyperuricemia
uric acid
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Summary:The final product of purine bases degradation in humans, reptiles and other primates is uric acid. The serum level of uric acid can be influenced by diet, certain systemic pathologies and a decreased renal excretion. Xanthine oxidase (XO) catalyzes the formation of uric acid with generation of reactive oxygen species (ROS), being active in physiological stress and ischemia. Uric acid has an antioxidant role at the extracellular level, but also in certain biological fluids such as saliva. In the intracellular environment of endothelial cells it plays a prooxidant role in conditions of hyperuricemia, contributing to the decrease of nitric oxide (NO) level, leading to endothelial dysfunction and the development of hypertension. The purpose of this review is to present the synthesis and biological effects of uric acid, the effects of hyperuricemia on NO production, and the link between hyperuricemia, endothelial dysfunction and hypertension.
ISSN:1842-8258
2069-6108
DOI:10.37897/RJMP.2020.2.10