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Uric acid modulates vascular endothelial function through the down regulation of nitric oxide production

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Uric acid modulates vascular endothelial function through the down regulation of nitric oxide production. / Papežíková, I; Pekarová, M; Kolářová, H; Klinke, A; Lau, D; Baldus, S; Lojek, A; Kubala, L.

In: FREE RADICAL RES, Vol. 47, No. 2, 02.2013, p. 82-88.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Papežíková, I, Pekarová, M, Kolářová, H, Klinke, A, Lau, D, Baldus, S, Lojek, A & Kubala, L 2013, 'Uric acid modulates vascular endothelial function through the down regulation of nitric oxide production', FREE RADICAL RES, vol. 47, no. 2, pp. 82-88. https://doi.org/10.3109/10715762.2012.747677

APA

Papežíková, I., Pekarová, M., Kolářová, H., Klinke, A., Lau, D., Baldus, S., Lojek, A., & Kubala, L. (2013). Uric acid modulates vascular endothelial function through the down regulation of nitric oxide production. FREE RADICAL RES, 47(2), 82-88. https://doi.org/10.3109/10715762.2012.747677

Vancouver

Papežíková I, Pekarová M, Kolářová H, Klinke A, Lau D, Baldus S et al. Uric acid modulates vascular endothelial function through the down regulation of nitric oxide production. FREE RADICAL RES. 2013 Feb;47(2):82-88. https://doi.org/10.3109/10715762.2012.747677

Bibtex

@article{2a1c1173d3464eb5ad9736cead299605,
title = "Uric acid modulates vascular endothelial function through the down regulation of nitric oxide production",
abstract = "Endothelial dysfunction characterized by decreased nitric oxide (NO) bioavailability is the first stage of coronary artery disease. It is known that one of the factors associated with an increased risk of coronary artery disease is a high plasma level of uric acid. However, causative associations between hyperuricaemia and cardiovascular risk have not been definitely proved. In this work, we tested the effect of uric acid on endothelial NO bioavailability. Electrochemical measurement of NO production in acetylcholine-stimulated human umbilical endothelial cells (HUVECs) revealed that uric acid markedly decreases NO release. This finding was confirmed by organ bath experiments on mouse aortic segments. Uric acid dose-dependently reduced endothelium-dependent vasorelaxation. To reveal the mechanism of decreasing NO bioavailability we tested the effect of uric acid on reactive oxygen species production by HUVECs, on arginase activity, and on acetylcholine-induced endothelial NO synthase phosphorylation. It was found that uric acid increases arginase activity and reduces endothelial NO synthase phosphorylation. Interestingly, uric acid significantly increased intracellular superoxide formation. In conclusion, uric acid decreases NO bioavailability by means of multiple mechanisms. This finding supports the idea of a causal association between hyperuricaemia and cardiovascular risk.",
keywords = "Acetylcholine/pharmacology, Animals, Arginase/metabolism, Cell Line, Coronary Artery Disease/metabolism, Down-Regulation, Endothelium, Vascular/metabolism, Human Umbilical Vein Endothelial Cells, Humans, Hyperuricemia/metabolism, Male, Mice, Mice, Inbred C57BL, Nitric Oxide/biosynthesis, Nitric Oxide Synthase Type III/metabolism, Phosphorylation, Reactive Oxygen Species/chemistry, Superoxides/metabolism, Uric Acid/blood",
author = "I Pape{\v z}{\'i}kov{\'a} and M Pekarov{\'a} and H Kol{\'a}{\v r}ov{\'a} and A Klinke and D Lau and S Baldus and A Lojek and L Kubala",
year = "2013",
month = feb,
doi = "10.3109/10715762.2012.747677",
language = "English",
volume = "47",
pages = "82--88",
journal = "FREE RADICAL RES",
issn = "1071-5762",
publisher = "informa healthcare",
number = "2",

}

RIS

TY - JOUR

T1 - Uric acid modulates vascular endothelial function through the down regulation of nitric oxide production

AU - Papežíková, I

AU - Pekarová, M

AU - Kolářová, H

AU - Klinke, A

AU - Lau, D

AU - Baldus, S

AU - Lojek, A

AU - Kubala, L

PY - 2013/2

Y1 - 2013/2

N2 - Endothelial dysfunction characterized by decreased nitric oxide (NO) bioavailability is the first stage of coronary artery disease. It is known that one of the factors associated with an increased risk of coronary artery disease is a high plasma level of uric acid. However, causative associations between hyperuricaemia and cardiovascular risk have not been definitely proved. In this work, we tested the effect of uric acid on endothelial NO bioavailability. Electrochemical measurement of NO production in acetylcholine-stimulated human umbilical endothelial cells (HUVECs) revealed that uric acid markedly decreases NO release. This finding was confirmed by organ bath experiments on mouse aortic segments. Uric acid dose-dependently reduced endothelium-dependent vasorelaxation. To reveal the mechanism of decreasing NO bioavailability we tested the effect of uric acid on reactive oxygen species production by HUVECs, on arginase activity, and on acetylcholine-induced endothelial NO synthase phosphorylation. It was found that uric acid increases arginase activity and reduces endothelial NO synthase phosphorylation. Interestingly, uric acid significantly increased intracellular superoxide formation. In conclusion, uric acid decreases NO bioavailability by means of multiple mechanisms. This finding supports the idea of a causal association between hyperuricaemia and cardiovascular risk.

AB - Endothelial dysfunction characterized by decreased nitric oxide (NO) bioavailability is the first stage of coronary artery disease. It is known that one of the factors associated with an increased risk of coronary artery disease is a high plasma level of uric acid. However, causative associations between hyperuricaemia and cardiovascular risk have not been definitely proved. In this work, we tested the effect of uric acid on endothelial NO bioavailability. Electrochemical measurement of NO production in acetylcholine-stimulated human umbilical endothelial cells (HUVECs) revealed that uric acid markedly decreases NO release. This finding was confirmed by organ bath experiments on mouse aortic segments. Uric acid dose-dependently reduced endothelium-dependent vasorelaxation. To reveal the mechanism of decreasing NO bioavailability we tested the effect of uric acid on reactive oxygen species production by HUVECs, on arginase activity, and on acetylcholine-induced endothelial NO synthase phosphorylation. It was found that uric acid increases arginase activity and reduces endothelial NO synthase phosphorylation. Interestingly, uric acid significantly increased intracellular superoxide formation. In conclusion, uric acid decreases NO bioavailability by means of multiple mechanisms. This finding supports the idea of a causal association between hyperuricaemia and cardiovascular risk.

KW - Acetylcholine/pharmacology

KW - Animals

KW - Arginase/metabolism

KW - Cell Line

KW - Coronary Artery Disease/metabolism

KW - Down-Regulation

KW - Endothelium, Vascular/metabolism

KW - Human Umbilical Vein Endothelial Cells

KW - Humans

KW - Hyperuricemia/metabolism

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Nitric Oxide/biosynthesis

KW - Nitric Oxide Synthase Type III/metabolism

KW - Phosphorylation

KW - Reactive Oxygen Species/chemistry

KW - Superoxides/metabolism

KW - Uric Acid/blood

U2 - 10.3109/10715762.2012.747677

DO - 10.3109/10715762.2012.747677

M3 - SCORING: Journal article

C2 - 23136942

VL - 47

SP - 82

EP - 88

JO - FREE RADICAL RES

JF - FREE RADICAL RES

SN - 1071-5762

IS - 2

ER -