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...
Main Authors: | , , , , , , , , , , , , , , , , , , |
---|---|
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 |