Exacerbation of adverse cardiovascular effects of aircraft noise in an animal model of arterial hypertension

Arterial hypertension is the most important risk factor for the development of cardiovascular disease. Recently, aircraft noise has been shown to be associated with elevated blood pressure, endothelial dysfunction, and oxidative stress. Here, we investigated the potential exacerbated cardiovascular...

Full description

Bibliographic Details
Main Authors: Sebastian Steven, Katie Frenis, Sanela Kalinovic, Miroslava Kvandova, Matthias Oelze, Johanna Helmstädter, Omar Hahad, Konstantina Filippou, Kamil Kus, Chiara Trevisan, Klaus-Dieter Schlüter, Kerstin Boengler, Stefan Chlopicki, Katrin Frauenknecht, Rainer Schulz, Mette Sorensen, Andreas Daiber, Swenja Kröller-Schön, Thomas Münzel
Format: Article
Language:English
Published: Elsevier 2020-07-01
Series:Redox Biology
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S2213231720302809
id doaj-30146d90574c4e3fad69d3fc14efc0a7
record_format Article
collection DOAJ
language English
format Article
sources DOAJ
author Sebastian Steven
Katie Frenis
Sanela Kalinovic
Miroslava Kvandova
Matthias Oelze
Johanna Helmstädter
Omar Hahad
Konstantina Filippou
Kamil Kus
Chiara Trevisan
Klaus-Dieter Schlüter
Kerstin Boengler
Stefan Chlopicki
Katrin Frauenknecht
Rainer Schulz
Mette Sorensen
Andreas Daiber
Swenja Kröller-Schön
Thomas Münzel
spellingShingle Sebastian Steven
Katie Frenis
Sanela Kalinovic
Miroslava Kvandova
Matthias Oelze
Johanna Helmstädter
Omar Hahad
Konstantina Filippou
Kamil Kus
Chiara Trevisan
Klaus-Dieter Schlüter
Kerstin Boengler
Stefan Chlopicki
Katrin Frauenknecht
Rainer Schulz
Mette Sorensen
Andreas Daiber
Swenja Kröller-Schön
Thomas Münzel
Exacerbation of adverse cardiovascular effects of aircraft noise in an animal model of arterial hypertension
Redox Biology
Environmental noise exposure
Arterial hypertension
Vascular oxidative stress
Inflammation
Endothelial function
author_facet Sebastian Steven
Katie Frenis
Sanela Kalinovic
Miroslava Kvandova
Matthias Oelze
Johanna Helmstädter
Omar Hahad
Konstantina Filippou
Kamil Kus
Chiara Trevisan
Klaus-Dieter Schlüter
Kerstin Boengler
Stefan Chlopicki
Katrin Frauenknecht
Rainer Schulz
Mette Sorensen
Andreas Daiber
Swenja Kröller-Schön
Thomas Münzel
author_sort Sebastian Steven
title Exacerbation of adverse cardiovascular effects of aircraft noise in an animal model of arterial hypertension
title_short Exacerbation of adverse cardiovascular effects of aircraft noise in an animal model of arterial hypertension
title_full Exacerbation of adverse cardiovascular effects of aircraft noise in an animal model of arterial hypertension
title_fullStr Exacerbation of adverse cardiovascular effects of aircraft noise in an animal model of arterial hypertension
title_full_unstemmed Exacerbation of adverse cardiovascular effects of aircraft noise in an animal model of arterial hypertension
title_sort exacerbation of adverse cardiovascular effects of aircraft noise in an animal model of arterial hypertension
publisher Elsevier
series Redox Biology
issn 2213-2317
publishDate 2020-07-01
description Arterial hypertension is the most important risk factor for the development of cardiovascular disease. Recently, aircraft noise has been shown to be associated with elevated blood pressure, endothelial dysfunction, and oxidative stress. Here, we investigated the potential exacerbated cardiovascular effects of aircraft noise in combination with experimental arterial hypertension. C57BL/6J mice were infused with 0.5 mg/kg/d of angiotensin II for 7 days, exposed to aircraft noise for 7 days at a maximum sound pressure level of 85 dB(A) and a mean sound pressure level of 72 dB(A), or subjected to both stressors. Noise and angiotensin II increased blood pressure, endothelial dysfunction, oxidative stress and inflammation in aortic, cardiac and/or cerebral tissues in single exposure models. In mice subjected to both stressors, most of these risk factors showed potentiated adverse changes. We also found that mice exposed to both noise and ATII had increased phagocytic NADPH oxidase (NOX-2)-mediated superoxide formation, immune cell infiltration (monocytes, neutrophils and T cells) in the aortic wall, astrocyte activation in the brain, enhanced cytokine signaling, and subsequent vascular and cerebral oxidative stress. Exaggerated renal stress response was also observed. In summary, our results show an enhanced adverse cardiovascular effect between environmental noise exposure and arterial hypertension, which is mainly triggered by vascular inflammation and oxidative stress. Mechanistically, noise potentiates neuroinflammation and cerebral oxidative stress, which may be a potential link between both risk factors. The results indicate that a combination of classical (arterial hypertension) and novel (noise exposure) risk factors may be deleterious for cardiovascular health.
topic Environmental noise exposure
Arterial hypertension
Vascular oxidative stress
Inflammation
Endothelial function
url http://www.sciencedirect.com/science/article/pii/S2213231720302809
work_keys_str_mv AT sebastiansteven exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
AT katiefrenis exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
AT sanelakalinovic exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
AT miroslavakvandova exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
AT matthiasoelze exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
AT johannahelmstadter exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
AT omarhahad exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
AT konstantinafilippou exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
AT kamilkus exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
AT chiaratrevisan exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
AT klausdieterschluter exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
AT kerstinboengler exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
AT stefanchlopicki exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
AT katrinfrauenknecht exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
AT rainerschulz exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
AT mettesorensen exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
AT andreasdaiber exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
AT swenjakrollerschon exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
AT thomasmunzel exacerbationofadversecardiovasculareffectsofaircraftnoiseinananimalmodelofarterialhypertension
_version_ 1724481522599198720
spelling doaj-30146d90574c4e3fad69d3fc14efc0a72020-11-25T03:52:40ZengElsevierRedox Biology2213-23172020-07-0134101515Exacerbation of adverse cardiovascular effects of aircraft noise in an animal model of arterial hypertensionSebastian Steven0Katie Frenis1Sanela Kalinovic2Miroslava Kvandova3Matthias Oelze4Johanna Helmstädter5Omar Hahad6Konstantina Filippou7Kamil Kus8Chiara Trevisan9Klaus-Dieter Schlüter10Kerstin Boengler11Stefan Chlopicki12Katrin Frauenknecht13Rainer Schulz14Mette Sorensen15Andreas Daiber16Swenja Kröller-Schön17Thomas Münzel18Center for Cardiology, Cardiology I – Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany; Center for Thrombosis and Hemostasis, University Medical Center of the Johannes Gutenberg-University, Mainz, GermanyCenter for Cardiology, Cardiology I – Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, GermanyCenter for Cardiology, Cardiology I – Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, GermanyCenter for Cardiology, Cardiology I – Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, GermanyCenter for Cardiology, Cardiology I – Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, GermanyCenter for Cardiology, Cardiology I – Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, GermanyCenter for Cardiology, Cardiology I – Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, GermanyCenter for Cardiology, Cardiology I – Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, GermanyJagiellonian Centre for Experimental Therapeutics (JCET), Jagiellonian University, Krakow, PolandInstitute of Neuropathology, University Hospital, Zurich, SwitzerlandDepartment of Physiology, Justus-Liebig University Gießen, GermanyDepartment of Physiology, Justus-Liebig University Gießen, GermanyJagiellonian Centre for Experimental Therapeutics (JCET), Jagiellonian University, Krakow, Poland; Chair of Pharmacology, Jagiellonian University Medical College, Krakow, PolandInstitute of Neuropathology, University Hospital, Zurich, SwitzerlandDepartment of Physiology, Justus-Liebig University Gießen, GermanyDanish Cancer Society, Copenhagen, Denmark; Department of Natural Science and Environment, Roskilde University, Roskilde, DenmarkCenter for Cardiology, Cardiology I – Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany; Corresponding authors. Center for Cardiology, Cardiology I – Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany.Center for Cardiology, Cardiology I – Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, GermanyCenter for Cardiology, Cardiology I – Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany; German Center for Cardiovascular Research (DZHK), Partner Site Rhine-Main, Mainz, Germany; Corresponding authors. Center for Cardiology, Cardiology I – Laboratory of Molecular Cardiology, University Medical Center of the Johannes Gutenberg-University, Mainz, Germany.Arterial hypertension is the most important risk factor for the development of cardiovascular disease. Recently, aircraft noise has been shown to be associated with elevated blood pressure, endothelial dysfunction, and oxidative stress. Here, we investigated the potential exacerbated cardiovascular effects of aircraft noise in combination with experimental arterial hypertension. C57BL/6J mice were infused with 0.5 mg/kg/d of angiotensin II for 7 days, exposed to aircraft noise for 7 days at a maximum sound pressure level of 85 dB(A) and a mean sound pressure level of 72 dB(A), or subjected to both stressors. Noise and angiotensin II increased blood pressure, endothelial dysfunction, oxidative stress and inflammation in aortic, cardiac and/or cerebral tissues in single exposure models. In mice subjected to both stressors, most of these risk factors showed potentiated adverse changes. We also found that mice exposed to both noise and ATII had increased phagocytic NADPH oxidase (NOX-2)-mediated superoxide formation, immune cell infiltration (monocytes, neutrophils and T cells) in the aortic wall, astrocyte activation in the brain, enhanced cytokine signaling, and subsequent vascular and cerebral oxidative stress. Exaggerated renal stress response was also observed. In summary, our results show an enhanced adverse cardiovascular effect between environmental noise exposure and arterial hypertension, which is mainly triggered by vascular inflammation and oxidative stress. Mechanistically, noise potentiates neuroinflammation and cerebral oxidative stress, which may be a potential link between both risk factors. The results indicate that a combination of classical (arterial hypertension) and novel (noise exposure) risk factors may be deleterious for cardiovascular health.http://www.sciencedirect.com/science/article/pii/S2213231720302809Environmental noise exposureArterial hypertensionVascular oxidative stressInflammationEndothelial function