Reactive Oxygen Species Are Central Mediators of Vascular Dysfunction and Hypertension Induced by Ethanol Consumption

Consumption of high amounts of ethanol is a risk factor for development of cardiovascular diseases such as arterial hypertension. The hypertensive state induced by ethanol is a complex multi-factorial event, and oxidative stress is a pathophysiological hallmark of vascular dysfunction associated wit...

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Published inAntioxidants Vol. 12; no. 10; p. 1813
Main Authors Padovan, Júlio C, Dourado, Thales M. H, Pimenta, Gustavo F, Bruder-Nascimento, Thiago, Tirapelli, Carlos R
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 29.09.2023
MDPI
Subjects
Acetaldehyde
Adipose tissue
Adipose tissues
Alcohol
Alcohol, Denatured
Alcoholism
Aldosterone
Angiotensin
Bioavailability
Blood pressure
Body mass index
Calcium (intracellular)
Cardiovascular diseases
Corticosteroids
Endothelium
Enzymes
Ethanol
Gender
Hypertension
NAD(P)H oxidase
NADPH oxidase
NADPH-diaphorase
Niacinamide
Nitric oxide
Oxidases
Oxidative stress
Public health
Reactive oxygen species
Renin
Review
Risk factors
Australia
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Abstract Consumption of high amounts of ethanol is a risk factor for development of cardiovascular diseases such as arterial hypertension. The hypertensive state induced by ethanol is a complex multi-factorial event, and oxidative stress is a pathophysiological hallmark of vascular dysfunction associated with ethanol consumption. Increasing levels of reactive oxygen species (ROS) in the vasculature trigger important processes underlying vascular injury, including accumulation of intracellular Ca2+ ions, reduced bioavailability of nitric oxide (NO), activation of mitogen-activated protein kinases (MAPKs), endothelial dysfunction, and loss of the anticontractile effect of perivascular adipose tissue (PVAT). The enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase plays a central role in vascular ROS generation in response to ethanol. Activation of the renin–angiotensin–aldosterone system (RAAS) is an upstream mechanism which contributes to NADPH oxidase stimulation, overproduction of ROS, and vascular dysfunction. This review discusses the mechanisms of vascular dysfunction induced by ethanol, detailing the contribution of ROS to these processes. Data examining the association between neuroendocrine changes and vascular oxidative stress induced by ethanol are also reviewed and discussed. These issues are of paramount interest to public health as ethanol contributes to blood pressure elevation in the general population, and it is linked to cardiovascular conditions and diseases.
AbstractList Consumption of high amounts of ethanol is a risk factor for development of cardiovascular diseases such as arterial hypertension. The hypertensive state induced by ethanol is a complex multi-factorial event, and oxidative stress is a pathophysiological hallmark of vascular dysfunction associated with ethanol consumption. Increasing levels of reactive oxygen species (ROS) in the vasculature trigger important processes underlying vascular injury, including accumulation of intracellular Ca2+ ions, reduced bioavailability of nitric oxide (NO), activation of mitogen-activated protein kinases (MAPKs), endothelial dysfunction, and loss of the anticontractile effect of perivascular adipose tissue (PVAT). The enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase plays a central role in vascular ROS generation in response to ethanol. Activation of the renin-angiotensin-aldosterone system (RAAS) is an upstream mechanism which contributes to NADPH oxidase stimulation, overproduction of ROS, and vascular dysfunction. This review discusses the mechanisms of vascular dysfunction induced by ethanol, detailing the contribution of ROS to these processes. Data examining the association between neuroendocrine changes and vascular oxidative stress induced by ethanol are also reviewed and discussed. These issues are of paramount interest to public health as ethanol contributes to blood pressure elevation in the general population, and it is linked to cardiovascular conditions and diseases.
Consumption of high amounts of ethanol is a risk factor for development of cardiovascular diseases such as arterial hypertension. The hypertensive state induced by ethanol is a complex multi-factorial event, and oxidative stress is a pathophysiological hallmark of vascular dysfunction associated with ethanol consumption. Increasing levels of reactive oxygen species (ROS) in the vasculature trigger important processes underlying vascular injury, including accumulation of intracellular Ca[sup.2+] ions, reduced bioavailability of nitric oxide (NO), activation of mitogen-activated protein kinases (MAPKs), endothelial dysfunction, and loss of the anticontractile effect of perivascular adipose tissue (PVAT). The enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase plays a central role in vascular ROS generation in response to ethanol. Activation of the renin–angiotensin–aldosterone system (RAAS) is an upstream mechanism which contributes to NADPH oxidase stimulation, overproduction of ROS, and vascular dysfunction. This review discusses the mechanisms of vascular dysfunction induced by ethanol, detailing the contribution of ROS to these processes. Data examining the association between neuroendocrine changes and vascular oxidative stress induced by ethanol are also reviewed and discussed. These issues are of paramount interest to public health as ethanol contributes to blood pressure elevation in the general population, and it is linked to cardiovascular conditions and diseases.
Consumption of high amounts of ethanol is a risk factor for development of cardiovascular diseases such as arterial hypertension. The hypertensive state induced by ethanol is a complex multi-factorial event, and oxidative stress is a pathophysiological hallmark of vascular dysfunction associated with ethanol consumption. Increasing levels of reactive oxygen species (ROS) in the vasculature trigger important processes underlying vascular injury, including accumulation of intracellular Ca 2+ ions, reduced bioavailability of nitric oxide (NO), activation of mitogen-activated protein kinases (MAPKs), endothelial dysfunction, and loss of the anticontractile effect of perivascular adipose tissue (PVAT). The enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase plays a central role in vascular ROS generation in response to ethanol. Activation of the renin–angiotensin–aldosterone system (RAAS) is an upstream mechanism which contributes to NADPH oxidase stimulation, overproduction of ROS, and vascular dysfunction. This review discusses the mechanisms of vascular dysfunction induced by ethanol, detailing the contribution of ROS to these processes. Data examining the association between neuroendocrine changes and vascular oxidative stress induced by ethanol are also reviewed and discussed. These issues are of paramount interest to public health as ethanol contributes to blood pressure elevation in the general population, and it is linked to cardiovascular conditions and diseases.
Audience Academic
Author Dourado, Thales M. H
Tirapelli, Carlos R
Padovan, Júlio C
Pimenta, Gustavo F
Bruder-Nascimento, Thiago
AuthorAffiliation 3 Departamento de Enfermagem Psiquiátrica e Ciências Humanas, Laboratório de Farmacologia, Escola de Enfermagem de Ribeirão Preto, University of São Paulo, Ribeirão Preto 14040-902, SP, Brazil
1 Laboratory of Blood and Vascular Biology, The Rockefeller University, New York, NY 10065, USA; padovaj@mail.rockefeller.edu
2 Programa de Pós-Graduação em Farmacologia, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo (USP), Ribeirão Preto 14040-902, SP, Brazil; thalesmhdourado97@usp.br (T.M.H.D.); gustavofelixpimenta@usp.br (G.F.P.)
4 Department of Pediatrics and Vascular Medicine Institute (VMI), University of Pittsburgh, Pittsburgh, PA 15260, USA; bruder@pitt.edu
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– name: 4 Department of Pediatrics and Vascular Medicine Institute (VMI), University of Pittsburgh, Pittsburgh, PA 15260, USA; bruder@pitt.edu
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Current address: Escola de Enfermagem de Ribeirão Preto, University of São Paulo, Ribeirão Preto 14040-902, SP, Brazil.
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Snippet Consumption of high amounts of ethanol is a risk factor for development of cardiovascular diseases such as arterial hypertension. The hypertensive state...
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proquest
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crossref
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Open Access Repository
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StartPage 1813
SubjectTerms Acetaldehyde
Adipose tissue
Adipose tissues
Alcohol
Alcohol, Denatured
Alcoholism
Aldosterone
Angiotensin
Bioavailability
Blood pressure
Body mass index
Calcium (intracellular)
Cardiovascular diseases
Corticosteroids
Endothelium
Enzymes
Ethanol
Gender
Hypertension
NAD(P)H oxidase
NADPH oxidase
NADPH-diaphorase
Niacinamide
Nitric oxide
Oxidases
Oxidative stress
Public health
Reactive oxygen species
Renin
Review
Risk factors
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Title Reactive Oxygen Species Are Central Mediators of Vascular Dysfunction and Hypertension Induced by Ethanol Consumption
URI https://www.proquest.com/docview/2882267169
https://search.proquest.com/docview/2883576383
https://pubmed.ncbi.nlm.nih.gov/PMC10604002
https://doaj.org/article/e628b6391567411182ca651aba82c4eb
Volume 12
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