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...
| Main Authors: | , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Amaltea Medical Publishing House
2020-06-01
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| Series: | Romanian Journal of Medical Practice |
| Subjects: | |
| Online Access: | https://rjmp.com.ro/articles/2020.2/RJMP_2020_2_Art-10.pdf |
| 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. |
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| ISSN: | 1842-8258 2069-6108 |