scholarly journals Oxidative Stress Mediates the Fetal Programming of Hypertension by Glucocorticoids

Antioxidants ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 531
Author(s):  
Jeremy Lamothe ◽  
Sandhya Khurana ◽  
Sujeenthar Tharmalingam ◽  
Chad Williamson ◽  
Collin J. Byrne ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Superoxide Dismutase ◽  
Fetal Programming ◽  
Cardiovascular Health ◽  
Phenylalanine Hydroxylase ◽  
Epigallocatechin Gallate ◽  
Female Offspring ◽  
Glutathione Peroxidase 1 ◽  
Protein Levels

The field of cardiovascular fetal programming has emphasized the importance of the uterine environment on postnatal cardiovascular health. Studies have linked increased fetal glucocorticoid exposure, either from exogenous sources (such as dexamethasone (Dex) injections), or from maternal stress, to the development of adult cardiovascular pathologies. Although the mechanisms are not fully understood, alterations in gene expression driven by altered oxidative stress and epigenetic pathways are implicated in glucocorticoid-mediated cardiovascular programming. Antioxidants, such as the naturally occurring polyphenol epigallocatechin gallate (EGCG), or the superoxide dismutase (SOD) 4-hydroxy-TEMPO (TEMPOL), have shown promise in the prevention of cardiovascular dysfunction and programming. This study investigated maternal antioxidant administration with EGCG or TEMPOL and their ability to attenuate the fetal programming of hypertension via Dex injections in WKY rats. Results from this study indicate that, while Dex-programming increased blood pressure in male and female adult offspring, administration of EGCG or TEMPOL via maternal drinking water attenuated Dex-programmed increases in blood pressure, as well as changes in adrenal mRNA and protein levels of catecholamine biosynthetic enzymes phenylalanine hydroxylase (PAH), tyrosine hydroxylase (TH), dopamine beta hydroxylase (DBH), and phenylethanolamine N-methyltransferase (PNMT), in a sex-specific manner. Furthermore, programmed male offspring displayed reduced antioxidant glutathione peroxidase 1 (Gpx1) expression, increased superoxide dismutase 1 (SOD1) and catalase (CAT) expression, and increased pro-oxidant NADPH oxidase activator 1 (Noxa1) expression in the adrenal glands. In addition, prenatal Dex exposure alters expression of epigenetic regulators histone deacetylase (HDAC) 1, 5, 6, 7, 11, in male and HDAC7 in female offspring. These results suggest that glucocorticoids may mediate the fetal programming of hypertension via alteration of epigenetic machinery and oxidative stress pathways.

scholarly journals Controllable oxidative stress and tissue specificity in major tissues during the torpor–arousal cycle in hibernating Daurian ground squirrels

Open Biology ◽  
2018 ◽  
Vol 8 (10) ◽  
pp. 180068 ◽  
Author(s):  
Yanhong Wei ◽  
Jie Zhang ◽  
Shenhui Xu ◽  
Xin Peng ◽  
Xia Yan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Superoxide Dismutase ◽  
Tissue Specificity ◽  
Kidney Tissue ◽  
Underlying Mechanism ◽  
Ground Squirrels ◽  
Glutathione Peroxidase 1 ◽  
Protein Levels ◽  
Gpx Activity ◽  
Superoxide Dismutase 2

Mammalian hibernators experience repeated hypoxic ischaemia and reperfusion during the torpor–arousal cycle. We investigated levels of oxidative stress, antioxidant capacity, and the underlying mechanism in heart, liver, brain and kidney tissue as well as plasma during different periods of hibernation in Daurian ground squirrels ( Spermophilus dauricus ). Our data showed that the levels of hydrogen peroxide significantly increased in the heart and brain during late torpor (LT) compared with levels during the summer active (SA) state. The content of malondialdehyde (MDA) was significantly lower during interbout arousal (IBA) and early torpor (ET) than that during SA or pre-hibernation (PRE), and MDA levels in the LT brain were significantly higher than the levels in other states. Superoxide dismutase 2 protein levels increased markedly in the heart throughout the entire torpor–arousal cycle. Catalase expression remained at an elevated level in the liver during the hibernation cycle. Superoxide dismutase 1 and glutathione peroxidase 1 (GPx1) expression increased considerably in all tissues during the IBA and ET states. In addition, the activities of the various antioxidant enzymes were higher in all tissues during IBA and ET than during LT; however, GPx activity in plasma decreased significantly during the hibernation season. The expression of p-Nrf2 decreased in all tissue types during IBA, but significantly increased during LT, especially in liver tissue. Interestingly, most changed indicators recovered to SA or PRE levels in post-hibernation (POST). These results suggest that increased reactive oxygen species during LT may activate the Nrf2/Keap1 antioxidant pathway and may contribute to the decreased MDA levels found during the IBA and ET states, thereby protecting organisms from oxidative damage over the torpor-arousal cycle of hibernation. This is the first report on the remarkable controllability of oxidative stress and tissue specificity in major oxidative tissues of a hibernator.

scholarly journals The Effect of Rice Bran Extract on Arterial Blood Pressure, Hepatic Steatosis, and Inflammation in Mice Fed with a High-Fat Diet

2020 ◽  
Vol 2020 ◽  
pp. 1-9 ◽  
Author(s):  
Naphatsanan Duansak ◽  
Pritsana Piyabhan ◽  
Umarat Srisawat ◽  
Jarinyaporn Naowaboot ◽  
Nusiri Lerdvuthisopon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Diastolic Blood Pressure ◽  
Arterial Blood Pressure ◽  
High Fat Diet ◽  
High Fat ◽  
Protein Levels ◽  
Arterial Blood ◽  
Cox 2 ◽  
And Oxidative Stress

Background. Inflammation and hypertension are primary mechanisms involving in obesity-associated adverse effects of a high-fat diet. The aim of this study was to evaluate the effects of rice bran extract (RBE) on arterial blood pressure, hepatic steatosis, inflammation, and oxidative stress in high-fat diet (HFD)-induced obese mice. Methods. Male ICR mice were divided into four groups, including a normal-diet control group, a high-fat diet (HFD) (60% kcal from fat) group, an HFD group treated with RBE (220 mg/kg/day), and an HFD group treated with 1100 mg/kg/day for eight weeks. Besides body weight and arterial blood pressure, we determined liver values of total cholesterol, triglyceride, as well as percent body fat, tumor necrosis factor-α (TNF-α), malondialdehyde (MDA), nuclear factor kappa-B (NF-κB), matrix metalloprotease-9 (MMP-9), cyclooxygenase-2 (COX-2), and mRNA endothelial nitric oxide synthase (eNOS). Results. The HFD group had increased body weight, increased systolic and diastolic blood pressure, liver total cholesterol, triglyceride, NF-κB, COX-2 and MMP-9 protein levels, and decreased mRNA eNOS in the aorta. Mice of the HFD group receiving RBE had reduced diastolic blood pressure, as well as significantly decreased liver and serum TNF-α and MDA levels in the liver, and reduced NF-κB levels in both the liver and heart. Conclusions. These results demonstrate that RBE decreases diastolic blood pressure, the liver lipid droplet accumulation, liver and myocardial NF-κB, myocardial COX-2 and MMP-9 protein levels, and oxidative stress. Moreover, RBE may improve endothelial function and may alleviate adverse health effects associated with obesity including obesity-associated hypertension.

scholarly journals DNA Damage in Lymphocytes in Hypertensive Subjects in Bangladesh

2013 ◽  
Vol 5 (3) ◽  
pp. 535-543
Author(s):  
M. Saiedullah ◽  
S. Hayat ◽  
M. R. Zamir ◽  
M. Arif ◽  
Z. H. Howlader ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Dna Damage ◽  
Superoxide Dismutase ◽  
Oxidative Dna Damage ◽  
Protein Carbonyl ◽  
Protein Carbonyl Content ◽  
Ribonucleic Acids ◽  
Stress Oxidative ◽  
Bangladeshi Population

Oxidative stress due to imbalance between the production of reactive oxygen species and their dismutation is claimed to be higher in hypertensive subjects than normotensive subjects. In hypertensive subjects oxidative stress may damage deoxy-ribonucleic acids (DNA). In this study plasma superoxide dismutase (SOD) activities, protein carbonyl contents (PCCs) and extent of DNA damage in lymphocytes were measured in specimens obtained from 86 subjects to compare oxidative stress and oxidative DNA damage between normotensive and hypertensive subjects and to assess their relationship with the degree of blood pressure. Results were expressed as mean±SD. Two-tailed unpaired t test and Pearson’s correlation test were done to compare or to determine the relationship between groups or variables. SOD activities were 2.85±0.12 unit/mg protein and 3.84±0.45 unit/mg protein (p<0.05) in hypertensive and normotensive groups respectively. PCCs were 4.77±0.36 nmol/mg protein and 3.75±0.23 nmol/mg protein in hypertensive and normotensive groups respectively. Olive tail moments (OTM) were 124.7±11.69 units and 108.9±9.27 units in hypertensive and normotensive groups respectively. The correlation coefficient of OTM was 0.3924 (p<0.05) for diastolic blood pressure and 0.3618 (p<0.05) for systolic blood pressure. Oxidative stress and DNA damage was higher in hypertensives than normotensives and DNA damage correlated positively with blood pressure. Keywords: Superoxide dismutase, Protein carbonyl content, Oxidative stress, Oxidative DNA damage, Hypertension, Bangladeshi population. © 2013 JSR Publications. ISSN: 2070-0237 (Print); 2070-0245 (Online). All rights reserved. doi: http://dx.doi.org/10.3329/jsr.v5i3.15022 J. Sci. Res. 5 (3), 535-543 (2013)  

scholarly journals Magnesium Lithospermate B Downregulates the Levels of Blood Pressure, Inflammation, and Oxidative Stress in Pregnant Rats with Hypertension

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Kaixiang Xu ◽  
Xiaohong Zang ◽  
Mian Peng ◽  
Qian Zhao ◽  
Binbin Lin
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Gestational Hypertension ◽  
Protective Effects ◽  
Urine Protein ◽  
Pregnant Rats ◽  
Protein Levels ◽  
Arterial Blood ◽  
Magnesium Lithospermate B ◽  
And Oxidative Stress

Background. Magnesium lithospermate B (MLB) was shown to suppress oxidative stress and reduce hypertension, but the role of MLB in pregnancy-induced hypertension (PIH) remains unknown. The objective of this study was to demonstrate the effects of MLB on rats with PIH. Methods. A total of 40 pregnant SD rats were selected, and 30 rats were orally given NG-nitro-L-arginine methyl ester (L-NAME, 60 mg/kg/day) to establish PIH rat models. Rats were equally divided into four groups: control, PIH, 5 mg/kg MLB, and 10 mg/kg MLB. MLB was consecutively administered into PIH rats for one week. The effects of MLB on mean arterial blood pressure (MAP), urine protein level, inflammation, and oxidative stress together with angiogenesis were analyzed. Results. MLB prevented the elevation in MAP and urine protein levels induced by L-NAME. The activities of inflammatory cytokines were highly increased in serum and placental tissues of PIH rats, while cotreatment with MLB partially reversed the activities of these cytokines. MLB also recovered the expression of reactive oxygen species (ROS) in plasma of PIH rats together with levels of oxidative stress and antioxidant capacity in the placenta of PIH rats. The decreased expressions of vascular endothelial growth factor (VEGF), endothelial nitric oxide synthase (eNOS), and NO observed in PIH rats were increased by MLB. In addition, 10 mg/kg MLB exhibited higher protective effects as compared to lower doses of 5 mg/kg. Conclusion. This study demonstrated that pretreatment with MLB decreased MAP, inflammation, and oxidative stress in rats with gestational hypertension.

scholarly journals Modulation of Hippocampal Antioxidant Defense System in Chronically Stressed Rats by Lithium

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Nataša Popović ◽  
Vesna Stojiljković ◽  
Snežana Pejić ◽  
Ana Todorović ◽  
Ivan Pavlović ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Superoxide Dismutase ◽  
Enzyme Activities ◽  
Manganese Superoxide Dismutase ◽  
Lithium Treatment ◽  
Antioxidant Defense System ◽  
Redox Balance ◽  
Preclinical Research ◽  
Protein Levels

This study examined the effects of lithium on gene expression and activity of the antioxidant enzymes copper zinc superoxide dismutase (SOD1), manganese superoxide dismutase (SOD2), catalase (CAT), glutathione peroxidase (GPx), and glutathione reductase (GR) in the hippocampus of chronically stressed rats. In addition, we examined the effects of lithium on anxiety behaviors, hippocampal concentrations of dopamine (DA) and malondialdehyde (MDA), protein levels of brain-derived neurotrophic factor (BDNF), tyrosine hydroxylase (TH), dopamine transporter (DAT), and catechol-O-methyltransferase (COMT), as well as activity of monoamine oxidase (MAO) in chronically stressed rats. The investigated parameters were quantified by real-time RT-PCR, Western blot analyses, and assays of enzyme activities. We found that lithium did not change gene expression of SOD1, CAT, GPx, and GR but decreased gene expression of SOD2 in chronically stressed rats. A very important result in this study was that lithium treatment decreased the enzyme activities of SOD1 and SOD2 but increased the enzyme activities of GPx and GR in stress condition, which indicates the control of redox balance. The reduced concentration of MDA confirms this. In addition, we found that lithium treatment decreased high protein levels of BDNF and DAT in chronically stressed rats to the level found in unstressed animals. Also, lithium treatment increased the expression of TH but decreased the enzyme activity of MAO B, which contributed to the increase of hippocampal concentration of DA in chronically stressed rats to the level of unstressed animals. Finally, lithium treatment in animals exposed to chronic stress increased the time spent in open arms. Lithium-induced modulation of hippocampal antioxidant status and attenuation of oxidative stress stabilized behavior in animals with high anxiety index. In addition, reduced oxidative stress was followed by the changes of both turnover of DA and levels of BDNF protein in chronically stressed rats treated with lithium. These findings may be important in preclinical research of the effects of lithium on oxidative stress level in pathological conditions.

scholarly journals Induction of 1-cys peroxiredoxin expression by oxidative stress in lung epithelial cells

2003 ◽  
Vol 285 (2) ◽  
pp. L363-L369 ◽  
Author(s):  
Han-Suk Kim ◽  
Yefim Manevich ◽  
Sheldon I. Feinstein ◽  
Jhang Ho Pak ◽  
Ye Shih Ho ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Enzyme Induction ◽  
Cysteine Residue ◽  
Lung Epithelial Cells ◽  
Transcriptional Level ◽  
Glutathione Peroxidase 1 ◽  
Protein Levels ◽  
Rat Lungs ◽  
Lung Epithelial ◽  
Mouse Lungs

1-Cys peroxiredoxin (1-cysPrx), a member of the peroxiredoxin family that contains a single conserved cysteine residue, reduces a broad spectrum of hydroperoxides. We studied changes in 1-cysPrx expression in rat lungs and lung cell lines in response to oxidative stress due to hyperoxia, H2O2, or paraquat. After 60 h of hyperoxia (>95% O2), mRNA and protein levels of 1-cysPrx and peroxidase activity were significantly elevated in rat lungs by ∼1.5- to 2-fold compared with the control ( P < 0.05). A similar induction of 1-cysPrx was observed in mouse lungs following exposure to O2 for 63 or 72 h; enzyme induction in mouse lungs was similar for wild-type and glutathione peroxidase 1 gene-targeted mice. H2O2 and paraquat treatment induced 1-cysPrx gene expression in L2 cells. Enzyme induction was attenuated by pretreatment with Trolox or N-acetylcysteine. Actinomycin D treatment showed that stability of 1-cysPrx mRNA was not altered in the presence of H2O2 or paraquat, indicating that increased expression with oxidative stress is regulated at the transcriptional level. These data indicate that the antioxidant enzyme 1-cysPrx is induced in lung cells by oxidative stress.

scholarly journals Evaluation of the Effects ofPinus koraiensisNeedle Extracts on Serum Lipid and Oxidative Stress in Adults with Borderline Dyslipidemia: A Randomized, Double-Blind, and Placebo-Controlled Clinical Trial

2016 ◽  
Vol 2016 ◽  
pp. 1-6
Author(s):  
Hansongyi Lee ◽  
Hyerang Kim ◽  
Ryowon Choue ◽  
Hyunjung Lim
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Superoxide Dismutase ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Blood Cholesterol ◽  
Low Density ◽  
Vldl Cholesterol ◽  
Before And After ◽  
And Oxidative Stress

Background.Dyslipidemia has been well-known as a common metabolic disorder contributing to cardiovascular disease. The aim of this study was to evaluate the effect of thePinus koraiensisneedle extracts (PKE) on the blood cholesterol and oxidative stress.Method.We conducted a 12-week randomized, double-blinded controlled trial to examine the effect of PKE on blood lipid profiles in adults with borderline dyslipidemia. Thirty-three eligible persons were recruited and randomly assigned into PKE (n=20) and placebo groups (n=13). Serum lipids including total cholesterol, low-density lipoprotein- (LDL-) cholesterol, high-density lipoprotein- (HDL-) cholesterol, very low-density lipoprotein- (VLDL-) cholesterol, and triglyceride were measured before and after trial. Serum insulin, glucose, and antioxidant indicators were also analyzed before and after trial and anthropometry and blood pressure were measured every 4 weeks.Results.After 12 weeks, PKE statically significant decreases in systolic blood pressure (p<0.05) and waist circumference (p<0.05) were observed. Also, VLDL-cholesterol significantly decreased (from24.4±10.0 mg/dL at baseline to18.4±4.1 mg/dL after 12 weeks) (p<0.05) and superoxide dismutase (SOD) increased (6.12±0.41 U/mL to9.06±0.62 U/mL) (p<0.01) in PKE group. However, after adjustment with WC, VLDL-cholesterol was not significant between groups (p=0.095) and while SOD remained significant between groups (p=0.013).Conclusion.The results show that PKE was effective in improving the superoxide dismutase in the individuals with borderline dyslipidemia.

scholarly journals IL-17-mediated oxidative stress is an important stimulator of AT1-AA and hypertension during pregnancy

2012 ◽  
Vol 303 (4) ◽  
pp. R353-R358 ◽  
Author(s):  
Pushpinder Dhillion ◽  
Kedra Wallace ◽  
Florian Herse ◽  
Jeremy Scott ◽  
Gerd Wallukat ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Superoxide Dismutase ◽  
Drinking Water ◽  
Interleukin 17 ◽  
Type I ◽  
Receptor Blockade ◽  
Induced Hypertension ◽  
Ad Libitum ◽  
Placental Oxidative Stress

Preeclampsia is associated with autoimmune cells TH17, secreting interleukin-17, autoantibodies activating the angiotensin II type I receptor (AT1-AA), and placental oxidative stress (ROS). The objective of our study was to determine whether chronic IL-17 increases blood pressure by stimulating ROS and AT1-AAs during pregnancy. To answer this question four groups of rats were examined: normal pregnant (NP, n = 20), NP+IL-17 ( n = 12), NP+tempol (4-hydroxy-2,2,6,6-tetramethylpiperidine- N-oxyl) ( n = 7) (a superoxide dismutase mimetic that scavenges ROS), and NP+IL-17+tempol ( n = 11). IL-17 (150 pg/day) was infused into NP rats while tempol was administered via the drinking water ad libitum. On day 19 blood pressure (MAP) was recorded, and plasma, urine, and tissue were collected for isolation of ROS detected by chemilluminescent technique. Urinary isoprostane was measured by ELISA. AT1-AAs were determined via cardiomyocyte assay and expressed as beats per minute. MAP increased from 98 ± 3 mmHg in NP to 123 ± 3 mmHg in IL-17-infused NP rats. Urinary isoprostane increased from 1,029 ± 1 in NP to 3,526 ± 2 pg·mg−1·day−1 in IL-17-infused rats ( P < 0.05). Placental ROS was 436 ± 4 RLU·ml−1·min−1 ( n = 4) in NP and 702 ± 5 ( n = 5) RLU·ml−1·min−1 in IL-17-treated rats. Importantly, AT1-AA increased from 0.41 ± 0.05 beats/min in NP rats ( n = 8) to 18.4 ± 1 beats/min in IL-17 rats ( n = 12). Administration of tempol attenuated the hypertension (101 ± 3 mmHg) ROS (459 ± 5 RLU·ml−1·min−1) and blunted AT1-AAs (7.3 ± 0.6 beats/min) in NP+IL-17+tempol-treated rats. Additionally, AT1 receptor blockade inhibited IL-17-induced hypertension and placental oxidative stress. MAP was 105 ± 5 mmHg and ROS was 418 ± 5 RLU·ml−1·min−1 in NP+IL 17-treated with losartan. These data indicate that IL-17 causes placental oxidative stress, which serves as stimulus modulating AT1-AAs that may play an important role in mediating IL-17-induced hypertension during pregnancy.

P4478Noise pollution exacerbates the development of arterial hypertension via additive oxidative stress and impairment of NO signaling

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Steven ◽  
K Frenis ◽  
S Kroeller-Schoen ◽  
S Kalinovic ◽  
J Helmstaedter ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Endothelial Dysfunction ◽  
Sound Pressure ◽  
Cardiovascular Health ◽  
Noise Exposure ◽  
Pressure Level ◽  
Aircraft Noise ◽  
Pressure Measurements ◽  
Additive Increase

Abstract Background Environmental noise pollution has been identified as a cardiovascular risk and is characterized by moderate hypertension, endothelial dysfunction, increased oxidative stress, and inflammation. We have gained insights into the mechanism by which these consequences occur by exposing mice lacking the critical NADPH oxidase subunit gp91phox to aircraft noise. Mice were protected from the effects of aircraft noise exposure. NADPH oxidase is believed to be the mediator by which angiotensin II increases oxidative stress, making investigation into the additive effect of noise and hypertension an important subject in modern cardiovascular health research. Methods and results C57Bl/6J mice were implanted with subcutaneous osmotic mini-pumps, delivering a moderate dose of 0.5mg/kg/d of angiotensin II for 7 days. Immediately following the implantation, half the mice were 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), a level at which hearing loss does not occur*. Non-invasive blood pressure measurements revealed an additive increase in blood pressure in noise-exposed hypertensive mice. Following sacrifice, endothelial dysfunction was evaluated through isometric tension recordings of 3mm aortic ring segments. These recordings support the blood pressure measurements and indicate a more serious impairment in acetylcholine-induced vasorelaxation in hypertensive mice exposed to noise than the hypertensive or noise only controls. Whole blood stimulated with phorbol 12,13-dibutyrate (PDBu) or zymosan A showed an additive increase in oxidative burst in in noise-exposed hypertensive mice. Dihydroethidium (DHE) staining was used to assess the presence of vascular and cerebral oxidative stress, showing similar additive effects in mice with hypertension plus noise exposure. High performance liquid chromatography (HPLC) measurement of 2-hydroxyethidium further confirmed additive increase of oxidative stress in the aorta and brain. Western blot analysis of aortic tissue revealed highest levels of gp91phox in mice with hypertension plus noise exposure and indicated a decrease in the ratio of P-eNOSSer1177:eNOS as well as a decrease in the ratio of eNOS dimer:monomer, exposing eNOS uncoupling as a potential pathomechanism for endothelial dysfunction and gp91phox as a source for the oxidative stress.Ongoing immunohistochemical and flow cytometric investigations will characterize the role of immune cells in these adverse effects. Conclusion Herein, we present novel data demonstrating additive noise-induced cardiovascular consequences on developing hypertension. Noise has previously been established as a cardiovascular risk factor, but the effects have not been determined in pre-existing or developing cardiovascular disease. Our results show a cumulative effect between noise exposure and hypertension and forge an important link between environmental stressors and cardiovascular health. Acknowledgement/Funding Boehringer Ingelheim Foundation

Sign in / Sign up

Export Citation Format

Share Document