Endothelium-derived reactive oxygen species: Their relationship to endothelium-dependent hyperpolarization and vascular tone

Anthie Ellis, Christopher Triggle

Research output: Contribution to journalReview article

71 Citations (Scopus)

Abstract

Opinions on the role of reactive oxygen species (ROS) in the vasculature have shifted in recent years, such that they are no longer merely regarded as indicators of cellular damage or byproducts of metabolism - they may also be putative mediators of physiological functions. Hydrogen peroxide (H 2O2), in particular, can initiate vascular myocyte proliferation (and, incongruously, apoptosis), hyperplasia, cell adhesion, migration, and the regulation of smooth muscle tone. Endothelial cells express enzymes that produce ROS in response to various stimuli, and H2O 2 is a potent relaxant of vascular smooth muscle. H2O 2 itself can mediate endothelium-dependent relaxations in some vascular beds. Although nitric oxide (NO) is well recognized as an endothelium-derived dilator, it is also well established, particularly in the microvasculature, that another factor, endothelium-derived hyperpolarizing factor (EDHF), is a significant determinant of vasodilatory tone. This review primarily focuses on the hypothesis that H2O2 is an EDHF in resistance arteries. Putative endothelial sources of H2O 2 and the effects of H2O2 on potassium channels, calcium homeostasis, and vascular smooth muscle tone are discussed. Furthermore, given the perception that ROS can more likely elicit cytotoxic effects than perform signalling functions, the arguments for and against H 2O2 being an endogenous vasodilator are assessed.

Original languageEnglish
Pages (from-to)1013-1028
Number of pages16
JournalCanadian Journal of Physiology and Pharmacology
Volume81
Issue number11
DOIs
Publication statusPublished - Nov 2003
Externally publishedYes

Fingerprint

Endothelium
Blood Vessels
Reactive Oxygen Species
Vascular Smooth Muscle
R Factors
Potassium Channels
Microvessels
Vasodilator Agents
Cell Adhesion
Muscle Cells
Hydrogen Peroxide
Cell Movement
Hyperplasia
Smooth Muscle
Nitric Oxide
Homeostasis
Endothelial Cells
Arteries
Apoptosis
Calcium

Keywords

  • Endothelium
  • Endothelium-derived hyperpolarizing factor (EDHF)
  • Hydrogen peroxide (HO)
  • Reactive oxygen species
  • Relaxation

ASJC Scopus subject areas

  • Physiology
  • Pharmacology

Cite this

@article{fedb18572718442f9731267ce7f298ed,
title = "Endothelium-derived reactive oxygen species: Their relationship to endothelium-dependent hyperpolarization and vascular tone",
abstract = "Opinions on the role of reactive oxygen species (ROS) in the vasculature have shifted in recent years, such that they are no longer merely regarded as indicators of cellular damage or byproducts of metabolism - they may also be putative mediators of physiological functions. Hydrogen peroxide (H 2O2), in particular, can initiate vascular myocyte proliferation (and, incongruously, apoptosis), hyperplasia, cell adhesion, migration, and the regulation of smooth muscle tone. Endothelial cells express enzymes that produce ROS in response to various stimuli, and H2O 2 is a potent relaxant of vascular smooth muscle. H2O 2 itself can mediate endothelium-dependent relaxations in some vascular beds. Although nitric oxide (NO) is well recognized as an endothelium-derived dilator, it is also well established, particularly in the microvasculature, that another factor, endothelium-derived hyperpolarizing factor (EDHF), is a significant determinant of vasodilatory tone. This review primarily focuses on the hypothesis that H2O2 is an EDHF in resistance arteries. Putative endothelial sources of H2O 2 and the effects of H2O2 on potassium channels, calcium homeostasis, and vascular smooth muscle tone are discussed. Furthermore, given the perception that ROS can more likely elicit cytotoxic effects than perform signalling functions, the arguments for and against H 2O2 being an endogenous vasodilator are assessed.",
keywords = "Endothelium, Endothelium-derived hyperpolarizing factor (EDHF), Hydrogen peroxide (HO), Reactive oxygen species, Relaxation",
author = "Anthie Ellis and Christopher Triggle",
year = "2003",
month = "11",
doi = "10.1139/y03-106",
language = "English",
volume = "81",
pages = "1013--1028",
journal = "Canadian Journal of Physiology and Pharmacology",
issn = "0008-4212",
publisher = "National Research Council of Canada",
number = "11",

}

TY - JOUR

T1 - Endothelium-derived reactive oxygen species

T2 - Their relationship to endothelium-dependent hyperpolarization and vascular tone

AU - Ellis, Anthie

AU - Triggle, Christopher

PY - 2003/11

Y1 - 2003/11

N2 - Opinions on the role of reactive oxygen species (ROS) in the vasculature have shifted in recent years, such that they are no longer merely regarded as indicators of cellular damage or byproducts of metabolism - they may also be putative mediators of physiological functions. Hydrogen peroxide (H 2O2), in particular, can initiate vascular myocyte proliferation (and, incongruously, apoptosis), hyperplasia, cell adhesion, migration, and the regulation of smooth muscle tone. Endothelial cells express enzymes that produce ROS in response to various stimuli, and H2O 2 is a potent relaxant of vascular smooth muscle. H2O 2 itself can mediate endothelium-dependent relaxations in some vascular beds. Although nitric oxide (NO) is well recognized as an endothelium-derived dilator, it is also well established, particularly in the microvasculature, that another factor, endothelium-derived hyperpolarizing factor (EDHF), is a significant determinant of vasodilatory tone. This review primarily focuses on the hypothesis that H2O2 is an EDHF in resistance arteries. Putative endothelial sources of H2O 2 and the effects of H2O2 on potassium channels, calcium homeostasis, and vascular smooth muscle tone are discussed. Furthermore, given the perception that ROS can more likely elicit cytotoxic effects than perform signalling functions, the arguments for and against H 2O2 being an endogenous vasodilator are assessed.

AB - Opinions on the role of reactive oxygen species (ROS) in the vasculature have shifted in recent years, such that they are no longer merely regarded as indicators of cellular damage or byproducts of metabolism - they may also be putative mediators of physiological functions. Hydrogen peroxide (H 2O2), in particular, can initiate vascular myocyte proliferation (and, incongruously, apoptosis), hyperplasia, cell adhesion, migration, and the regulation of smooth muscle tone. Endothelial cells express enzymes that produce ROS in response to various stimuli, and H2O 2 is a potent relaxant of vascular smooth muscle. H2O 2 itself can mediate endothelium-dependent relaxations in some vascular beds. Although nitric oxide (NO) is well recognized as an endothelium-derived dilator, it is also well established, particularly in the microvasculature, that another factor, endothelium-derived hyperpolarizing factor (EDHF), is a significant determinant of vasodilatory tone. This review primarily focuses on the hypothesis that H2O2 is an EDHF in resistance arteries. Putative endothelial sources of H2O 2 and the effects of H2O2 on potassium channels, calcium homeostasis, and vascular smooth muscle tone are discussed. Furthermore, given the perception that ROS can more likely elicit cytotoxic effects than perform signalling functions, the arguments for and against H 2O2 being an endogenous vasodilator are assessed.

KW - Endothelium

KW - Endothelium-derived hyperpolarizing factor (EDHF)

KW - Hydrogen peroxide (HO)

KW - Reactive oxygen species

KW - Relaxation

UR - http://www.scopus.com/inward/record.url?scp=0346729711&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0346729711&partnerID=8YFLogxK

U2 - 10.1139/y03-106

DO - 10.1139/y03-106

M3 - Review article

C2 - 14719036

AN - SCOPUS:0346729711

VL - 81

SP - 1013

EP - 1028

JO - Canadian Journal of Physiology and Pharmacology

JF - Canadian Journal of Physiology and Pharmacology

SN - 0008-4212

IS - 11

ER -