In:
Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2019 ( 2019-02-11), p. 1-8
Abstract:
Hydrogen peroxide, formed in the endothelium, acts as a factor contributing to the relaxation of blood vessels. The reason for this vasodilatory effect could be modulation by H 2 O 2 of calcium metabolism, since mobilization of calcium ions in endothelial cells is a trigger of endothelium-dependent relaxation. The aim of this work was to investigate the influence of H 2 O 2 on the effects of Ca 2+ -mobilizing agonists in human umbilical vein endothelial cells (HUVEC). We have found that H 2 O 2 in concentration range 10-100 μ M increases the rise of [Ca 2+ ] i induced by 5-hydroxytryptamine (5-HT) and carbachol and does not affect the calcium signals of ATP, agonist of type 1 protease-activated receptor SFLLRN, histamine and bradykinin. Using specific agonists of 5-HT1B and 5-HT2B receptors CGS12066B and BW723C86, we have demonstrated that H 2 O 2 potentiates the effects mediated by these types of 5-HT receptors. Potentiation of the effect of BW723C86 can be produced by the induction of endogenous oxidative stress in HUVEC. We have shown that the activation of 5-HT2B receptor by BW723C86 causes production of reactive oxygen species (ROS). Inhibitor of NADPH oxidases VAS2870 suppressed formation of ROS and partially inhibited [Ca 2+ ] i rise induced by BW723C86. Thus, it can be assumed that vasorelaxation induced by endogenous H 2 O 2 in endothelial cells partially occurs due to the potentiation of the agonist-induced calcium signaling.
Type of Medium:
Online Resource
ISSN:
1942-0900
,
1942-0994
DOI:
10.1155/2019/1701478
Language:
English
Publisher:
Hindawi Limited
Publication Date:
2019
detail.hit.zdb_id:
2455981-7
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