Essential Hypertension and Oxidative Stress: Novel Future Perspectives (original) (raw)
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Essential hypertension and oxidative stress: New insights
World Journal of Cardiology, 2014
Core tip: This review focuses on one of the most prevalent diseases worldwide: hypertension, providing new insights about the key role of oxidative stress in the pathophysiology of essential hypertension and new clinical attempts to demonstrate the usefulness of antioxidant therapy in the treatment of hypertension.
Evidences for oxidative stress in essential hypertension
Central European Journal of Medicine, 2012
Aim: This study explores the degree of oxidative stress in essential arterial hypertension (EAH). Even oxidative stress appears as one of several metabolic abnormalities involved in essential hypertension, it remains uncertain whether is primary or secondary. However measurement of the main oxidant may be useful in order to recognize and monitor oxidative stress. Methods: Lipid peroxidation products (TBA reac tive substances) were determined in red blood cells (RBC) and serum together with markers of antioxidant status: total antioxidative capacity (AOC), catalase activity (CAT) and RBC glutathione (GSH) content in four investigated groups. The first group consisted of regularly and adequately treated hyper tensive patients without complication (regulated), patients with hyper tension and complication of some organs and organic systems were the non-regulated group. Third group were patients at the beginning of EAH (non-treated) and controls were normotensive individuals. Results: Compared with controls, regulated and non-treated group, non-regulated hyper tensive pati ents had higher TBARS concen tration in plasma (p<0.001) and lower AOC, CAT activity without differences in GSH content. Conclusion: Recent findings suggest that hyper tension is a condition followed by intensive oxidative stress and reduced antioxidant factors. Adequate and strictly controlled therapy, hygienic and diet regime and possible use of antioxidants can signi fi cantly reduce blood pressure and prevent possible complications.
Relationship between Oxidative Stress and Essential Hypertension
Hypertension Research, 2007
This study investigated the association of blood pressure with blood oxidative stress-related parameters in normotensive and hypertensive subjects. A cross-sectional design was applied to 31 hypertensive patients and 35 healthy normotensive subjects. All subjects were men between the ages of 35 and 60 years. Exclusion criteria were obesity, dyslipidemia, diabetes mellitus, smoking and current use of any medication. All patients underwent 24-h ambulatory blood pressure monitoring and sampling of blood and urine. Antioxidant enzymes activity, reduced/oxidized glutathione ratio (GSH/GSSG), and lipid peroxidation (malondialdehyde) were determined in erythrocytes. Parameters measured in the plasma of test subjects were plasma antioxidant status, lipid peroxidation (8-isoprostane), plasma vitamin C and E, and the blood pressure modulators renin, aldosterone, endothelin-1 and homocysteine. Daytime systolic and diastolic blood pressures of hypertensives were negatively correlated with plasma antioxidant capacity (r =-0.46, p <0.009 and r =-0.48, p <0.007), plasma vitamin C levels (r =-0.53, p <0.003 and r =-0.44, p <0.02), erythrocyte activity of antioxidant enzymes, and erythrocyte GSH/GSSG ratio, with hypertensives showing higher levels of oxidative stress. Blood pressures showed a positive correlation with both plasma and urine 8-isoprostane. Neither plasma vitamin E nor the assessed blood pressure modulator levels showed significant differences between the groups or correlation with blood pressures. These findings demonstrate a strong association between blood pressure and some oxidative stress-related parameters and suggest a possible role of oxidative stress in the pathophysiology of essential hypertension. (Hypertens Res 2007; 30: 1159-1167)
Study of Oxidative Stress in Essential Hypertension
Biomedical and Pharmacology Journal, 2015
Essential hypertension is associated with an elevation of reactive oxygen species (ROS) which reacts with membrane lipids to form lipid hydroperoxides that decomposes to form Malondialdehyde (MDA) an indicator of oxidative stress. Endogenous antioxidant enzyme, Superoxide dismutase (SOD) counteracts oxidative stress. This study aims at understanding the role of oxidative stress in essential hypertension. The study comprised of 50 confirmed cases of hypertension and 50 age and sex matched controls .Inclusion criteria includes patients with blood pressure e" 140/90 mm of Hg, while patients with secondary hypertension, stroke, CAD,MI and diabetes mellitus are excluded. Serum SOD estimated spectrophotometrically by Mishra H.P. & Fridovich I,1972 method and Plasma MDA by colorimetric method of Satoch K.et al. SOD activity was statistically significantly (p<0.0001) decreased while MDA level was statistically significantly (p<0.0001) increased in hypertensives compared to controls. Patients suffering from hypertension have increased ROS activity which oxidizes nitric oxide (NO) and affect vascular tone.Lassegue et al (2004) also found convincing evidence that ROS is an intrinsic part of pathology of hypertension. If oxidative stress is indeed a cause or consequence of hypertension, then reduction in oxidative damage may result in a reduction in blood pressure. Antioxidants like Vit.A,Vit.C & Vit E which are present in vegetables, citrus fruits & oils respectively are able to trap ROS and thus may be capable of reducing oxidative damage and possibly blood pressure. Estimation of oxidative stress markers (SOD & MDA) is simple and inexpensive; it can be used to predict the development of atherosclerotic disease like coronary artery disease, cerebrovascular disease and renal complications associated with essential hypertension. Oxidative stress markers estimation may also be helpful in assessing the usefulness of antihypertensive drugs in prevention of associated complications.
Oxidative Stress Markers and Antioxidant Status in Human Hypertension
2011
Background: There is growing evidence that oxidative stress contributes to hypertension justified by observations, predominantly in animal models. Objective: The aim of the present study was to observe the relationship, if any, between systemic arterial hypertension and biochemical markers of oxidative stress, inflammation and aging. Materials & Methods: 50 subjects with hypertension and 50 age and sex-matched controls were included in the study. The nitrate-nitrite ratio, malondialdehyde (measured as thiobarbituric acid reactive substances, superoxide dismutase activity, and high sensitive C-Reactive Protein were assayed on samples from these subjects by standardized methodology. The data obtained was statistically analyzed. Results: Statistically significant mean values of serum nitrate-nitrite ratio and plasma superoxide dismutase activity were lower and that of serum malondialdehyde was higher in hypertensive subjects when compared to the controls. Serum nitrate-nitrite ratio, malondialdehyde and superoxide dismutase activity exhibited statistically significant multivariate correlation with each other while High Sensitive C-Reactive Protein was not significantly correlated. Nitrate-nitrite ratio was significantly lower with aging both in normotensive and hypertensive subjects. Conclusion: The present study confirmed the role of oxidation mediated tissue damage in generation of hypertension and suggested the usefulness of examining nitrate:nitrite ratio as a surrogate marker of the pathophysiologic process leading to generation of human hypertension. The study also confirmed an exacerbation of oxidative stress with advancement of age in both study groups.
Association of oxidative stress and endothelial dysfunction in hypertension
Analytical Biochemistry, 2020
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Study of Oxidative Stress Parameters in Hypertension and their Correlation with Blood Pressure
2014
Increasing evidence has underlined the importance of oxidative stress in the Pathophysiology of hypertension and its contribution to the associated complications. However the correlation between oxidative stress parameters and blood pressure levels is not clearly understood. Thus present study was done to evaluate the oxidative stress parameters in patients with hypertension and to check the correlation, if any, between these parameters and systolic and diastolic blood pressure. Plasma malondialdehyde, superoxide dismutase and catalase levels were measured in sixty hypertensive and forty normotensive subjects. Pearson’s correlation analysis was performed to study the correlation between these parameters and systolic and diastolic blood pressure. Enhanced oxidative stress was observed in hypertensive subjects as denoted by raised plasma malondialdehyde levels and reduced superoxide dismutase and catalase levels. Plasma malondialdehyde correlated positively whereas superoxide dismutas...
Circulation Journal, 2010
Oxidative stress is a key factor in the pathogenesis of hypertension and target organ damage, beginning in the earliest stages. Extensive evidence indicates that the pivotal role of oxidative stress in the pathogenesis of hypertension is due to its effects on the vasculature in relation to the development of atherosclerotic processes. It remains unclear, however, whether oxidative stress in the brain, particularly the autonomic nuclei (including the vasomotor center), has an important role in the occurrence and maintenance of hypertension via activation of the sympathetic nervous system. The aim of the present review is to describe the contribution of oxidative stress in the brain to the neural mechanisms that underlie hypertension, and discuss evidence that brain oxidative stress is a potential therapeutic target.
The Future Challenge of Reactive Oxygen Species (ROS) in Hypertension: From Bench to Bed Side
International Journal of Molecular Sciences, 2017
Reactive oxygen species (ROS) act as signaling molecules that control physiological processes, including cell adaptation to stress. Redox signaling via ROS has quite recently become the focus of much attention in numerous pathological contexts, including neurodegenerative diseases, kidney and cardiovascular disease. Imbalance in ROS formation and degradation has also been implicated in essential hypertension. Essential hypertension is characterized by multiple genetic and environmental factors which do not completely explain its associated risk factors. Thereby, even if advances in therapy have led to a significant reduction in hypertension-associated complications, to interfere with the unbalance of redox signals might represent an additional therapeutic challenge. The decrease of nitric oxide (NO) levels, the antioxidant activity commonly found in preclinical models of hypertension and the ability of antioxidant approaches to reduce ROS levels have spurred clinicians to investigate the contribution of ROS in humans. Indeed, particular effort has recently been devoted to understanding how redox signaling may contribute to vascular pathobiology in human hypertension. However, although biomarkers of oxidative stress have been found to positively correlate with blood pressure in preclinical model of hypertension, human data are less convincing. We herein provide an overview of the most relevant mechanisms via which oxidative stress might contribute to the pathophysiology of essential hypertension. Moreover, alternative approaches, which are directed towards improving antioxidant machinery and/or interfering with ROS production, are also discussed.
Oxidative-Nitrosative Stress In Hypertension
Current Vascular Pharmacology, 2005
Reactive oxygen species (ROS) are important signaling molecules in the vasculature. However, when there is imbalance between their occurrence and antioxidant defense mechanisms, ROS can contribute to the vascular abnormalities that lead to hypertension. Evidence accumulated in the last decade strongly supports the notion that ROS are generated in the vasculature mainly by NAD(P)H oxidase in a mechanism that is angiotensin II-dependent. Activation of this enzyme leads to superoxide production and uncouples endothedial NO synthase (eNOS), which sustains oxidative stress while increasing the levels of tissue-damaging peroxynitrite. The latter can result in vascular dysfunction. NAD(P)Hdependent ROS formation, in particular H 2 O 2 , could also contribute to vascular injury by sustaining NAD(P)H oxidase activation, promoting inflammatory gene expression, extracellular matrix reorganization, and growth (hypertrophy/hyperplasia) of vascular smooth muscle cells. The effect of ROS appears to be mediated by redox-sensitive targets such as tyrosine kinases and phosphatases, mitogen-activated protein kinases, transcription factors, matrix metalloproteinases, peroxisome proliferator activated receptor-α, poly(ADP-ribose)polymerase-1, Ca 2+ signaling mechanisms and secreted factors such as cyclophilin A and heat shock protein 90-α. Redox-sensitive targets appear to play a central role in normal vascular function, but can also lead to remodeling of the vascular wall, increasing vascular reactivity and hypertension. Polymorphisms in the p22phox gene promoter could determine susceptibility to NAD(P)H-mediated oxidative stress in humans and animals with hypertension. Although ROS are strongly implicated in the etiology of hypertension, clinical trials with antioxidants are inconclusive regarding their effectiveness in treating the disease. New drugs with both antihypertensive action and antioxidant properties (Celiprolol, Carvedilol) offer promising results in the management of hypertension.