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Exacerbation of Adverse Cardiovascular Effects of Aircraft Noise in an Animal Model of Arterial Hypertension

Abstract

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.

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References
1.
Wenzel P, Mollnau H, Oelze M, Schulz E, Wickramanayake J, Muller J . First evidence for a crosstalk between mitochondrial and NADPH oxidase-derived reactive oxygen species in nitroglycerin-triggered vascular dysfunction. Antioxid Redox Signal. 2008; 10(8):1435-47. DOI: 10.1089/ars.2007.1969. View

2.
Zhao H, Joseph J, Fales H, Sokoloski E, Levine R, Vasquez-Vivar J . Detection and characterization of the product of hydroethidine and intracellular superoxide by HPLC and limitations of fluorescence. Proc Natl Acad Sci U S A. 2005; 102(16):5727-32. PMC: 556312. DOI: 10.1073/pnas.0501719102. View

3.
Stawski L, Haines P, Fine A, Rudnicka L, Trojanowska M . MMP-12 deficiency attenuates angiotensin II-induced vascular injury, M2 macrophage accumulation, and skin and heart fibrosis. PLoS One. 2014; 9(10):e109763. PMC: 4193823. DOI: 10.1371/journal.pone.0109763. View

4.
Hausding M, Jurk K, Daub S, Kroller-Schon S, Stein J, Schwenk M . CD40L contributes to angiotensin II-induced pro-thrombotic state, vascular inflammation, oxidative stress and endothelial dysfunction. Basic Res Cardiol. 2013; 108(6):386. DOI: 10.1007/s00395-013-0386-5. View

5.
Forstermann U, Munzel T . Endothelial nitric oxide synthase in vascular disease: from marvel to menace. Circulation. 2006; 113(13):1708-14. DOI: 10.1161/CIRCULATIONAHA.105.602532. View