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

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00159816%3A_____%2F13%3A00060710" target="_blank" >RIV/00159816:_____/13:00060710 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/68081707:_____/13:00392583

Výsledek na webu

<a href="http://dx.doi.org/10.3109/10715762.2012.747677" target="_blank" >http://dx.doi.org/10.3109/10715762.2012.747677</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.3109/10715762.2012.747677" target="_blank" >10.3109/10715762.2012.747677</a>

Jazyk výsledku

angličtina

Název v původním jazyce

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

Popis výsledku v původním jazyce

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 ofuric 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 inacetylcholine-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 p

Název v anglickém jazyce

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

Popis výsledku anglicky

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 ofuric 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 inacetylcholine-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 p

Druh

J_x - Nezařazeno - Článek v odborném periodiku (Jimp, Jsc a Jost)

CEP obor

CE - Biochemie

OECD FORD obor

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Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Rok uplatnění

2013

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Free radical research

ISSN

1071-5762

e-ISSN

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Svazek periodika

47

Číslo periodika v rámci svazku

2

Stát vydavatele periodika

GB - Spojené království Velké Británie a Severního Irska

Počet stran výsledku

7

Strana od-do

82-88

Kód UT WoS článku

000313594600003

EID výsledku v databázi Scopus

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