Association between oxidative stress and blood pressure in Korean subclinical hypertensive patients

2013 ◽  
Vol 46 (2) ◽  
pp. 126 ◽  
Author(s):  
Jeong-Hwa Han ◽  
Hye-Jin Lee ◽  
Hee Jeong Choi ◽  
Kyung Eun Yun ◽  
Myung-Hee Kang
2019 ◽  
pp. 3
Author(s):  
Elsa Mathew ◽  
J.K. Mukkadan

Background: Cardiovascular disease is one of the leading causes of mortality and morbidity in India and worldwide. Hypertension is a major public health problem because of its high frequency and concomitant risk of cardiovascular disease, kidney disease, and stroke. World Health Organization named it a Silent killer as hypertension is asymptomatic during its clinical course. Experimental evidence supports a role for oxidative stress in vascular injury and hypertension. This study was undertaken, to compare the serum levels of malondialdehyde (MDA) and super-oxide dismutase (SOD) among normotensive, prehypertensive and hypertensive subjects. Materials and methods: In this cross-sectional study, 34 normotensives, 44 prehypertensive and 45 hypertensive subjects were included. The participants were subjected to selection protocol consisting of physical examination and biochemical analysis. All subjects underwent blood pressure measurement, total cholesterol, and oxidative stress marker estimation, especially SOD and MDA. The comparison of parameters between the group was carried out using One Way ANOVA. The correlation between the parameter was analyzed by Karl Pearson Correlation Coefficient using SPSS 20.0. Result : The MDA (nmol/ml) in normotensive, prehypertensive and hypertensive patients was 2.55±0.072, 3.43±0.44 and 4.01±0.37 respectively. SOD (U/ml) level in normotensive, prehypertensive and hypertensive patients was 13.47±1.96, 11.57±0.81, and 8.52±1.78 respectively. Systolic and diastolic blood pressure had a negative correlation with SOD. MDA levels show a positive correlation with systolic blood pressure and diastolic blood pressure. Total cholesterol had no significant with SOD and MDA. Conclusion: The present study showed a strong association of oxidative stress with systolic and diastolic blood pressure.


ESC CardioMed ◽  
2018 ◽  
pp. 2227-2229
Author(s):  
Hung-Fat Tse ◽  
Jo-Jo Hai

Hypertension is one of the most important independent risk factors for atrial fibrillation (AF). Conversely, AF is associated with an increased risk of stroke in hypertensive patients. While the pathophysiology linking the two conditions is not completely understood, it is likely attributed to interplay between mechanical stress, activation of the renin–angiotensin–aldosterone system, oxidative stress, and inflammatory response in hypertension to cause atrial electroanatomical remodelling, and thus AF. Management of hypertensive patients with AF encompasses lenient rate control, thromboprophylaxis, and good blood pressure control.


Pharmacia ◽  
2021 ◽  
Vol 68 (3) ◽  
pp. 705-711
Author(s):  
Zeina A. Althanoon ◽  
Isam H. Mahmood

The pathogenesis of essential hypertension through the interaction with elements of the rennin angiotensin aldosterone system is affected by oxidative stress and inflammation. The present study aimed to assess the effects of ACE-Inhibitor, lisinopril, on blood pressure, lipid profiles (total cholesterol, triglycerides, LDL and HDL), MDA, and TAS, hsCRP, and serum leptin levels n hypertensive patients. A case control study included 100 newly diagnosed mild to moderate hypertensive patients and another 100 apparently healthy aged and sex matched subjects as controls. The patients were treated with 10 mg lisinopril orally per day for three months’ duration. Venous blood sample was taken to test levels of MDA, GSH and TAS, hsCRP, lipid profiles and leptin in the serum before and after lisinopril therapy for both patients and controls. Systolic and diastolic blood pressure were also assessed before and after lisinopril therapy for both patients and controls. In hypertensive patients treated with lisinopril, markers of oxidative stress (MDA, TAS and GSH), high sensitive C-reactive protein and leptin were all found to be decreased significantly after drug treatment (p < 0.01). Lisinopril affectively lowered systolic and diastolic BP values (p < 0.01). A significant decrease in lipid profile (p < 0.01) with a significant increase in HDL-C and TAS levels (p < 0.01) were found in lisinopril treated group in comparison with their values before treatment. Lisinopril may be used as a treatment for high blood pressure, as well as for the insulin resistance, hyperleptinemic, and low-grade inflammatory states that are associated with the disease.


2020 ◽  
Vol 11 (2) ◽  
pp. 2614-2619
Author(s):  
Elsa Mathew ◽  
Mukkadan J. K.

Studies have evaluated that high blood pressure kills nine million people annually Persistent. Psychological factors can be considered as a primary threat to the increase of hypertension. It may lead to cardiovascular disease, stroke and kidney disease. The current work was conducted to analyze the disparity of anxiety, dyslipidemia and oxidative stress in pre-hypertensive and hypertensive subjects. This was a cross-sectional study conducted among 180 subjects. Based on the Joint National Committee 8 Criteria, participants were divided into hypertensive patients (n₌60) and pre-hypertensive patients (n₌63). Fifty-seven healthy subjects with normal blood pressure were served as the control group. Anthropometric measurements and blood pressure were measured using the standard procedure. The biochemical parameters for measuring oxidative stress, blood glucose levels, and lipid profile were estimated. Anxiety level was assessed with the State-trait anxiety inventory (STAI) questionnaire. It is observed that the serum MalonDiAldehyde (MDA) levels (nmol/ml) were significantly higher in pre-hypertensive (3.74±0.33) and hypertensive (4.7±0.38) compared to normotensive subjects (3.05±0.38). The Superoxide Dismutase (SOD) activity (U/ml) was higher in subjects with normal blood pressure (12.67±2.31) than pre-hypertensive (11.16±2.43) and hypertensive subjects (8.98±2.32). The MDA had a significant positive correlation, and SOD had a negative association with waist-hip ratio, systolic blood pressure, diastolic blood pressure, fasting blood sugar, high-density lipoprotein, and state and trait anxiety. The present study confirmed that pre-hypertensive and hypertensive subjects suffered from more oxidative stress than normotensive subjects.


2019 ◽  
Vol 12 (3) ◽  
pp. 253-259 ◽  
Author(s):  
Manish Kumar Verma ◽  
◽  
Anoop Jaiswal ◽  
Preeti Sharma ◽  
Pradeep Kumar ◽  
...  

Concurrent with the misbalance of oxidizing agents and antioxidants, high blood pressure is a major physical burden condition in the current scenario. Tumor necrosis factor-α (TNF-α) plays a vital role in the pathogenesis of hypertension. Tumor necrosis factor-α, inhibitor improves clinical symptoms however their outcome on high blood pressure has not been investigated. We investigated the inflammatory marker TNF-α, malondialdehyde (MDA) and ferric reducing antioxidant power (FRAP) in hypertensive patients. We measured randomly blood pressure using an ambulatory observe in hypertensive patients, measured systolic BP X 140 mmHg and/or diastolic BP X 90 mmHg were considered hypertensive. Total 60 cases were considered in the study that involves 30 hypertensive patients and 30 normal control. Measurements of serum concentrations of TNF-α, MDA, FRAP in hypertension patients was done in both the groups. Serum TNF-α was found to be remarkably increased in study subjects as compared to normal group (r=0.32, p<0.0001*). Serum MDA was also raised in hypertensive as compared to control (r=0.99**, p<0.0001*). While Serum FRAP was found to be decreased in hypertensive group in comparison to healthy control (r=0.23, p<0.0001*). It is concluded that high blood pressure leads to generation of oxidative stress with remarkable elevation of TNF-α and malondialdehyde levels. While reduced FRAP indicates its probable role in lipid peroxidation and in the pathogenesis of hypertension.


Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 798
Author(s):  
Francisco A. O. Júnior ◽  
Clara R. Ruiz ◽  
Yohanna Oliveira ◽  
Marco A. V. Barros ◽  
Alexandre S. Silva ◽  
...  

Exploring an alternative to improve the clinical management of hypertension, we tested the hypothesis that food supplementation with coconut oil (EVCO), alone or combined with aerobic exercise training, could exert an antihypertensive effect (primary outcome) in patients with stage 1 hypertension. Forty-five hypertensive volunteers of both genders participated in a placebo-controlled clinical trial. The volunteers were submitted to 24-hour ambulatory blood pressure monitoring, analysis of blood pressure variability (BPV), measurement of serum malondialdehyde (MDA) and nutritional assessment. Results indicate that EVCO consumption had no adverse effects. The supplementation did not increase the caloric intake compared with placebo, and the dietary constituents were similar between groups, except for the saturated fats, especially lauric acid. The analysis of blood pressure indicated absence of antihypertensive effect of EVCO alone or combined with physical training. Furthermore, no effects on blood pressure variability and oxidative stress were observed in the supplemented hypertensive patients. Thus, despite the results observed in pre-clinical studies, the current clinical study did not provide evidence to support the use of coconut oil as an adjuvant in the management of hypertension in humans.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
P Di Pietro ◽  
M Oliveti ◽  
E Sommella ◽  
A Damato ◽  
A Puca ◽  
...  

Abstract Background Sortilin, a member of vacuolar protein sorting domain family Vps10, has been positively correlated with vascular and metabolic disorders in humans. Previous study has shown that, in response to Fas receptor stimulation, sortilin together with acid sphingomyelinase (ASMase) promote the clustering of lipid rafts and subsequent activation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase in coronary endothelial cells. However, whether sortilin plays a role in endothelial cells function is currently unknown. Purpose To assess whether sortilin per se was able to influence vascular function, thereby contributing to the pathogenesis of cardiovascular diseases. Methods Pressure myography was used to study vascular reactivity of mesenteric arteries. To investigate the involvement of acid sphingomyelinase (ASM), we performed gene silencing approach and fluorometric activity assay. NADPH oxidase lucigenin assay was used to evaluate oxidative stress in endothelial cells and resistance vessels. The effects of circulating sortilin on cardiovascular system was evaluated by systemic delivery of recombinant sortilin protein to wild-type (WT), sphingosine-1-phosphate receptor 3 (S1P3) and NADPH oxidase 2 (gp91phox/NOX2) deficient mice. Systolic arterial blood pressure (SBP) was noninvasively registered in conscious mice by tail-cuff blood monitoring. Finally, to explore the translational relevance of sortilin, we measured sortilin and NOX2 soluble derived peptide levels using ELISA and quantified sphingosine-1-phosphate (S1P) by liquid chromatography–tandem mass spectrometry (LC-MS/MS) in plasma of hypertensive patients. Results Here we demonstrated that sortilin evoked endothelial dysfunction in mesenteric arteries due to increased NADPH oxidase-derived oxidative stress. Knockdown of ASM successfully prevented impairment of endothelial function. Using the inhibitor of sphingosine kinase type 1 (SphK1), sortilin failed to evoke endothelial impairment as well as NADPH oxidase activation. In endothelial cells, sortilin induced S1P-dependent activation of Rac1/NOX2 signaling axis, which was prevented by TY-52156, an antagonist of lysosphingolipid receptor S1P3. In vivo sortilin administration induced arterial hypertension in WT mice. In contrast, genetic deletion of S1P3 and gp91phox/NOX2 resulted in preservation of endothelial function and SBP unchanged levels after 14 days of systemic sortilin administration. Finally, to translate these research findings into a clinical setting, we found that hypertensive patients have higher plasma levels of sortilin, ASMase, S1P and soluble NOX2 derived peptide than normotensive subjects. Conclusions These results demonstrate the pathologic role of sortilin in the modulation of endothelial function and arterial blood pressure, suggesting that sortilin and its mediators might represent novel therapeutic targets in vascular diseases and hypertension. Funding Acknowledgement Type of funding source: None


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