The Influence of Nrf2 on Cardiac Responses to Environmental Stressors
Nrf2 protects the lung from adverse responses to oxidants, including 100% oxygen (hyperoxia) and airborne pollutants like particulate matter (PM) exposure, but the role of Nrf2 on heart rate (HR) and heart rate variability (HRV) responses is not known. We hypothesized that genetic disruption of Nrf2...
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doaj-e7c5d06b0701426887240a15913962162020-11-24T23:02:27ZengHindawi LimitedOxidative Medicine and Cellular Longevity1942-09001942-09942013-01-01201310.1155/2013/901239901239The Influence of Nrf2 on Cardiac Responses to Environmental StressorsReuben Howden0Eva Gougian1Marcus Lawrence2Samantha Cividanes3Wesley Gladwell4Laura Miller-DeGraff5Page H. Myers6D. Clay Rouse7Robert B. Devlin8Hye-Youn Cho9Steven R. Kleeberger10Laboratory of Systems Physiology, Department of Kinesiology, University of North Carolina at Charlotte, Charlotte, NC, USALaboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USALaboratory of Systems Physiology, Department of Kinesiology, University of North Carolina at Charlotte, Charlotte, NC, USALaboratory of Systems Physiology, Department of Kinesiology, University of North Carolina at Charlotte, Charlotte, NC, USALaboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USALaboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USAComparative Medicine Branch, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USADivision of Laboratory Animal Resources, Duke University Medical Center, Durham, NC, USAUnited States Environmental Protection Agency, Research Triangle Park, NC, USALaboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USALaboratory of Respiratory Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USANrf2 protects the lung from adverse responses to oxidants, including 100% oxygen (hyperoxia) and airborne pollutants like particulate matter (PM) exposure, but the role of Nrf2 on heart rate (HR) and heart rate variability (HRV) responses is not known. We hypothesized that genetic disruption of Nrf2 would exacerbate murine HR and HRV responses to severe hyperoxia or moderate PM exposures. Nrf2-/- and Nrf2+/+ mice were instrumented for continuous ECG recording to calculate HR and HRV (low frequency (LF), high frequency (HF), and total power (TP)). Mice were then either exposed to hyperoxia for up to 72 hrs or aspirated with ultrafine PM (UF-PM). Compared to respective controls, UF-PM induced significantly greater effects on HR (P<0.001) and HF HRV (P<0.001) in Nrf2-/- mice compared to Nrf2+/+ mice. Nrf2-/- mice tolerated hyperoxia significantly less than Nrf2+/+ mice (~22 hrs; P<0.001). Reductions in HR, LF, HF, and TP HRV were also significantly greater in Nrf2-/- compared to Nrf2+/+ mice (P<0.01). Results demonstrate that Nrf2 deletion increases susceptibility to change in HR and HRV responses to environmental stressors and suggest potential therapeutic strategies to prevent cardiovascular alterations.http://dx.doi.org/10.1155/2013/901239 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Reuben Howden Eva Gougian Marcus Lawrence Samantha Cividanes Wesley Gladwell Laura Miller-DeGraff Page H. Myers D. Clay Rouse Robert B. Devlin Hye-Youn Cho Steven R. Kleeberger |
spellingShingle |
Reuben Howden Eva Gougian Marcus Lawrence Samantha Cividanes Wesley Gladwell Laura Miller-DeGraff Page H. Myers D. Clay Rouse Robert B. Devlin Hye-Youn Cho Steven R. Kleeberger The Influence of Nrf2 on Cardiac Responses to Environmental Stressors Oxidative Medicine and Cellular Longevity |
author_facet |
Reuben Howden Eva Gougian Marcus Lawrence Samantha Cividanes Wesley Gladwell Laura Miller-DeGraff Page H. Myers D. Clay Rouse Robert B. Devlin Hye-Youn Cho Steven R. Kleeberger |
author_sort |
Reuben Howden |
title |
The Influence of Nrf2 on Cardiac Responses to Environmental Stressors |
title_short |
The Influence of Nrf2 on Cardiac Responses to Environmental Stressors |
title_full |
The Influence of Nrf2 on Cardiac Responses to Environmental Stressors |
title_fullStr |
The Influence of Nrf2 on Cardiac Responses to Environmental Stressors |
title_full_unstemmed |
The Influence of Nrf2 on Cardiac Responses to Environmental Stressors |
title_sort |
influence of nrf2 on cardiac responses to environmental stressors |
publisher |
Hindawi Limited |
series |
Oxidative Medicine and Cellular Longevity |
issn |
1942-0900 1942-0994 |
publishDate |
2013-01-01 |
description |
Nrf2 protects the lung from adverse responses to oxidants, including 100% oxygen (hyperoxia) and airborne pollutants like particulate matter (PM) exposure, but the role of Nrf2 on heart rate (HR) and heart rate variability (HRV) responses is not known. We hypothesized that genetic disruption of Nrf2 would exacerbate murine HR and HRV responses to severe hyperoxia or moderate PM exposures. Nrf2-/- and Nrf2+/+ mice were instrumented for continuous ECG recording to calculate HR and HRV (low frequency (LF), high frequency (HF), and total power (TP)). Mice were then either exposed to hyperoxia for up to 72 hrs or aspirated with ultrafine PM (UF-PM). Compared to respective controls, UF-PM induced significantly greater effects on HR (P<0.001) and HF HRV (P<0.001) in Nrf2-/- mice compared to Nrf2+/+ mice. Nrf2-/- mice tolerated hyperoxia significantly less than Nrf2+/+ mice (~22 hrs; P<0.001). Reductions in HR, LF, HF, and TP HRV were also significantly greater in Nrf2-/- compared to Nrf2+/+ mice (P<0.01). Results demonstrate that Nrf2 deletion increases susceptibility to change in HR and HRV responses to environmental stressors and suggest potential therapeutic strategies to prevent cardiovascular alterations. |
url |
http://dx.doi.org/10.1155/2013/901239 |
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