scholarly journals Contribution of captopril thiol group to the prevention of spontaneous hypertension

2007 ◽  
pp. S41-S48
Author(s):  
O Pecháňová
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Ace Inhibitors ◽  
Thiol Group ◽  
No Synthase ◽  
Spontaneous Hypertension ◽  
Cgmp Level ◽  
Control Group ◽  
No Production ◽  
Enalapril Group

We aimed to compare the effect of angiotensin converting enzyme (ACE) inhibitors captopril (containing thiol group) and enalapril (without thiol group) on the development of spontaneous hypertension and to analyze mechanisms of their actions, particularly effects on oxidative stress and NO production. Six-week-old SHR were divided into three groups: control, group receiving captopril (50 mg/kg/day) or enalapril (50 mg/kg/day) for 6 weeks. At the end of experiment, systolic blood pressure (SBP) increased by 41 % in controls. Both captopril and enalapril prevented blood pressure increase, however, SBP in the captopril group (121+/-5 mmHg) was significantly lower than that in the enalapril group (140+/-5 mmHg). Concentration of conjugated dienes in the aorta was significantly lower in the captopril group compared to the enalapril group. Captopril and enalapril increased NO synthase activity in the heart and aorta to the similar level. Neither captopril nor enalapril was, however, able to increase the expression of eNOS. Both ACE inhibitors increased the level of cGMP. However, cGMP level was significantly higher in the aorta of captopril group. We conclude that captopril, beside inhibition of ACE, prevented hypertension by increasing NO synthase activity and by simultaneous decrease of oxidative stress which resulted in increase of cGMP concentration.

Renal and pressor effects of aminoguanidine in cirrhotic rats with ascites.

1996 ◽  
Vol 7 (12) ◽  
pp. 2694-2699
Author(s):  
M C Ortíz ◽  
L A Fortepiani ◽  
C Martínez ◽  
N M Atucha ◽  
J García-Estañ
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Liver Cirrhosis ◽  
Experimental Model ◽  
Systemic Blood Pressure ◽  
Arterial Hypotension ◽  
Control Group ◽  
No Production ◽  
Water Excretion ◽  
Excretory Function

Recent work indicates that nitric oxide (NO) plays an important role in the systemic and renal alterations of liver cirrhosis. This study used aminoguanidine (AG), a preferential inhibitor of inducible nitric oxide synthase (iNOS), to evaluate the role of this NOS isoform in the systemic and renal alterations of an experimental model of liver cirrhosis with ascites (carbon tetrachloride/ phenobarbital). Experiments have been performed in anesthetized cirrhotic rats and their respective control rats prepared for clearance studies. Administration of AG (10 to 100 mg/kg, iv) elevated dose-dependent mean arterial pressure (MAP, in mm Hg) in the cirrhotic rats from a basal level of 79.3 +/- 3.6 to 115.0 +/- 4.7, whereas in the control animals, MAP increased only with the highest dose of the inhibitor (from 121.8 +/- 3.6 to 133.3 +/- 1.4). In the cirrhotic group, AG also significantly increased sodium and water excretion, whereas these effects were very modest in the control group. Plasma concentration of nitrates+nitrites, measured as an index of NO production, were significantly increased in the cirrhotic animals in the basal period and decreased with AG to levels not significantly different from the control animals. Similar experiments performed with the nonspecific NOS inhibitor N omega-nitro-L-arginine (NNA) also demonstrated an increased pressor sensitivity of the cirrhotic rats, but the arterial hypotension was completely corrected. These results, in an experimental model of liver cirrhosis with ascites, show that AG exerts a beneficial effect as a result of inhibition of NO production, increasing blood pressure and improving the reduced excretory function. Because NNA, but not AG, completely normalized the arterial hypotension, it is suggested that the constitutive NOS isoform is also contributing in an important degree. It is concluded that the activation of both inducible and constitutive NOS isoforms plays an important role in the lower systemic blood pressure and associated abnormalities that characterize liver cirrhosis.

scholarly journals A Subpressor Dose of Angiotensin II Elevates Blood Pressure in a Normotensive Rat Model by Oxidative Stress

2015 ◽  
pp. 153-159 ◽  
Author(s):  
M. M. GOVENDER ◽  
A. NADAR
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Angiotensin Ii ◽  
Mrna Expression ◽  
Rat Model ◽  
Wistar Rat ◽  
Control Group ◽  
Sod Activity ◽  
Male Wistar Rats ◽  
Experimental Group

Oxidative stress is an imbalance between free radicals and antioxidants, and is an important etiological factor in the development of hypertension. Recent experimental evidence suggests that subpressor doses of angiotensin II elevate oxidative stress and blood pressure. We aimed to investigate the oxidative stress related mechanism by which a subpressor dose of angiotensin II induces hypertension in a normotensive rat model. Normotensive male Wistar rats were infused with a subpressor dose of angiotensin II for 28 days. The control group was sham operated and infused with saline only. Plasma angiotensin II and H2O2 levels, whole-blood glutathione peroxidase, and AT-1a, Cu/Zn SOD, and p22phox mRNA expression in the aorta was assessed. Systolic and diastolic blood pressures were elevated in the experimental group. There was no change in angiotensin II levels, but a significant increase in AT-1a mRNA expression was found in the experimental group. mRNA expression of p22phox was increased significantly and Cu/Zn SOD decreased significantly in the experimental group. There was no significant change to the H2O2 and GPx levels. Angiotensin II manipulates the free radical-antioxidant balance in the vasculature by selectively increasing O2− production and decreasing SOD activity and causes an oxidative stress induced elevation in blood pressure in the Wistar rat.

scholarly journals Swimming Attenuates Blood Pressure and Oxidative Stress in Hypertensive Rats

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Anica Petkovic ◽  
Marko Ravic ◽  
Sasa Plecevic ◽  
Jovana Jeremic ◽  
Ivan Srejovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Diastolic Pressure ◽  
Control Group ◽  
Albino Rats ◽  
Positive System ◽  
Hypertensive Rats ◽  
Stress Markers ◽  
Antioxidant Parameters ◽  
And Oxidative Stress

Abstract Hypertension presents one of the main risk factors for cardiovascular diseases which are the leading cause of morbidity and mortality worldwide. Structural and mechanical changes of the heart and blood vessels as well as overproduction of reactive oxygen species may occur due to the increased blood pressure. Therewith, the goal of our study was to estimate the effects and duration of swimming as a possible therapy approach on blood pressure and oxidative stress parameters in normotensive and hypertensive rats. The study was conducted on 60 male Wistar albino rats divided into two groups, normotensive and hypertensive rats. Each of these groups was divided into three subgroups according to the swimming protocol. The swimming training was kept constant (60 min/day, for five days a week) with two days of rest. After six or nine weeks of the swimming protocol, blood pressure and oxidative stress markers were measured. The control group rats were put in water for one minute a day, in order to avoid water-induced stress. Training significantly reduced systolic blood pressure in hypertensive rats, while diastolic pressure did not change in the group that swam six or nine weeks. The results showed that swimming increases the activity of all measured antioxidative parameters, while values of prooxidants varied depending on the training protocol. Our results confirmed that swimming, as an aerobic exercise, decreases blood pressure and has time-dependent positive system adaptations, especially on the antioxidant parameters.

scholarly journals Lacidipine Ameliorates the Endothelial Senescence and Inflammatory Injury Through CXCR7/P38/C/EBP-β Signaling Pathway

2021 ◽  
Vol 8 ◽  
Author(s):  
Xing Liu ◽  
Zhuoshan Huang ◽  
Yuanyuan Zhang ◽  
Xing Shui ◽  
Fanmao Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Signaling Pathway ◽  
Cell Activity ◽  
Protective Role ◽  
Cell Counting ◽  
Control Group ◽  
Inflammatory Injury ◽  
Beneficial Effects

Background: Lacidipine, a third-generation calcium channel blocker, exerts beneficial effects on the endothelium of hypertensive patients in addition to blood pressure lowering. However, the detailed mechanism underlying Lacidipine-related endothelial protection is still elusive.Methods: Sixteen spontaneous hypertensive rats (SHRs) were randomly divided into two groups: Lacidipine-treated SHR group and saline-treated control group. Tail systolic blood pressure was monitored for four consecutive weeks. Endothelial cells (ECs) were pretreated with Lacidipine prior to being stimulated with H2O2, bleomycin, or Lipopolysaccharides (LPS) in vitro. Then, cell activity, migration, and senescence were measured by Cell Counting Kit-8 assay, transwell assay, and β-galactosidase staining, respectively. The fluorescent probe 2′, 7′-dichlorofluorescein diacetate (DCFH-DA) was used to assess the intracellular reactive oxygen species (ROS). Related protein expression was detected by Western blotting and immunofluorescence.Results: Our data showed that Lacidipine treatment lowered the blood pressure of SHRs accompanied by the elevation of CXCR7 expression and suppression of P38 and CCAAT/enhancer-binding protein beta (C/EBP-β) compared with the control group. In vitro experiments further demonstrated that Lacidipine increased the cell viability and function of ECs under oxidative stress, cell senescence, and inflammatory activation via the CXCR7/P38/signaling pathway.Conclusions: Our results suggested that Lacidipine plays a protective role in EC senescence, oxidative stress, and inflammatory injury through the regulation of CXCR7/P38/C/EBP-β signaling pathway.

Induction of Oxidative Stress by Glutathione Depletion Causes Severe Hypertension in Normal Rats

Hypertension ◽  
2000 ◽  
Vol 36 (suppl_1) ◽  
pp. 688-688
Author(s):  
Nosratola D Vaziri ◽  
Xiu Q Wang ◽  
Fariba Oveisi ◽  
Behdad Rad
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Drinking Water ◽  
Urinary Excretion ◽  
Antioxidant Therapy ◽  
Glutathione Depletion ◽  
Hepatic Tissue ◽  
Control Group ◽  
Sprague Dawley ◽  
Arterial Blood

59 Several recent studies have shown that certain forms of genetic and acquired hypertension (HTN) are associated with oxidative stress and respond favorably to antioxidant therapy. We hypothesize that oxidative stress, per se, may cause HTN via (among other mechanisms) enhanced oxidation and inactivation of nitric oxide (NO). To test this hypothesis, Sprague-Dawley rats were subjected to oxidative stress by glutathione (GSH) depletion using GSH synthase inhibitor, buthionine sulfoximine (BSO, 30 mmol/L in drinking water), for two weeks. The control group was given drug-free drinking water. In parallel experiments, subgroups of animals were provided vitamin E-fortified chow and vitamin C-supplemented drinking water. Arterial blood pressure, urinary excretion of NO metabolites (NO 2 +NO 3 , NOx), and liver tissue GSH were measured. In addition, plasma, kidney, heart, liver and aorta were tested by Western blot analysis for nitrotyrosine, which is the footprint of NO inactivation by reactive oxygen species (ROS). The BSO-treated group showed a three-fold fall in hepatic tissue GSH content (0.99±0.3 vs 3.4±0.3 μmol/g wet tissue, P<0.001), a marked elevation in blood pressure (203±3 vs 120±2 mmHg, P<0.001) and a significant reduction in urinary excretion of NO metabolites, nitrate + nitrite (316±23 vs 595±29 μmol/g creatinine, P<0.01), suggesting depressed NO availability. This was associated with a significant accumulation in all tested tissues of nitrotyrosine (P<0.05 for all comparisons). Administration of vitamins E+C ameliorated HTN (156±4 mmHg, P<0.01), improved urinary NOx excretion (392±28 μmol/g creatinine, P<0.05) and mitigated nitrotyrosine accumulation (despite persistent GSH depletion) in the BSO-treated animals. However, vitamins E+C treatment had no effect on any of the above parameters in the control group (data not shown). In conclusion, GSH depletion resulted in perturbation of the NO system and severe HTN in normal animals. The effects of BSO were mitigated by concomitant antioxidant therapy despite GSH depletion, supporting the notion that oxidative stress was involved in the pathogenesis of HTN in this model.

Wine polyphenols improve cardiovascular remodeling and vascular function in NO-deficient hypertension

2002 ◽  
Vol 282 (3) ◽  
pp. H942-H948 ◽  
Author(s):  
Iveta Bernátová ◽  
Olga Pechánová ◽  
Pavel Babál ◽  
Sona Kyselá ◽  
Svetoslav Stvrtina ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Myocardial Fibrosis ◽  
Vascular Function ◽  
Spontaneous Recovery ◽  
Left Ventricular ◽  
No Synthase ◽  
Control Group ◽  
Cross Sectional ◽  
Wine Polyphenols ◽  
Group A

The effects of the red wine polyphenolic compounds (Provinol) on hypertension, left ventricular hypertrophy, myocardial fibrosis, and vascular remodeling were investigated after chronic inhibition of nitric oxide (NO) synthase by administration of N G-nitro-l-arginine methyl ester (l-NAME) to rats. Rats were divided into four groups: a control group, a group treated for 4 wk with l-NAME (40 mg · kg−1 · day−1), and two groups treated with l-NAME followed by 3 wk of either spontaneous recovery or recovery with Provinol treatment (40 mg · kg−1 · day−1). Administration of Provinol produced a greater readiness of the decrease in blood pressure than that in the spontaneous recovery group. Provinol significantly depressed myocardial fibrosis and expedited the decrease in aortic cross-sectional area, the increase in endothelium-dependent relaxation, and the decrease in contraction of the aorta. These effects of Provinol were associated with a greater increase of NO synthase activity in the left ventricle and the aorta. The present study provides evidence that Provinol accelerates the regression of blood pressure and improves structural and functional cardiovascular changes produced by chronic inhibition of NO synthesis.

17β-Estradiol prevents oxidative stress and decreases blood pressure in ovariectomized rats

2000 ◽  
Vol 279 (5) ◽  
pp. R1599-R1605 ◽  
Author(s):  
Isabel Hernández ◽  
Juan L. Delgado ◽  
Julian Díaz ◽  
Tomas Quesada ◽  
M. José G. Teruel ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Total Antioxidant Status ◽  
Ovariectomized Rats ◽  
No Production ◽  
Estrogen Replacement ◽  
Lower Plasma ◽  
Vascular Conductance ◽  
Total Antioxidant ◽  
17Β Estradiol

In this study, we tested whether estrogen deficiency is associated with oxidative stress and decreased nitric oxide (NO) production, which could be responsible for an increased blood pressure in ovariectomized rats. Hemodynamic studies were performed on conscious, chronically instrumented rats. Chronic estrogen replacement on ovariectomized rats lowered blood pressure ∼13 mmHg, from 119 ± 3 mmHg in ovariectomized rats to 106 ± 3 mmHg in ovariectomized-treated rats; it was also accompanied by an increase in cardiac index and vascular conductance, achieving hemodynamic values similar to those shown by sham-operated rats. N G-nitro-l-arginine methyl ester administration lowered significantly less the vascular conductance (0.14 ± 0.01 vs. 0.22 ± 0.03 and 0.26 ± 0.01 ml · min−1 · mmHg−1/100 g; P < 0.05) in ovariectomized rats than in the sham-operated and estrogen-treated ovariectomized rats, respectively. Estrogen replacement prevented the lower plasma levels of nitrites/nitrates observed in ovariectomized rats. The lower plasma total antioxidant status and reduced thiol groups and the increase in plasma lipoperoxides presented in ovariectomized animals were reestablished with the estrogen treatment. These results show that estrogen administration decreases blood pressure and increases vascular conductance in ovariectomized rats. This effect may be related to an increase in NO synthesis and/or preventing oxidative stress, then improving endothelial function.

The Correlation of Anxiety, Dyslipidemia and Oxidative stress in Prehypertensive and Hypertensive patients

2020 ◽  
Vol 11 (2) ◽  
pp. 2614-2619
Author(s):  
Elsa Mathew ◽  
Mukkadan J. K.
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Trait Anxiety ◽  
Normal Blood ◽  
Control Group ◽  
National Committee ◽  
Normal Blood Pressure ◽  
Hypertensive Patients ◽  
Normotensive Subjects ◽  
And Oxidative Stress

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.

scholarly journals Heparanase Inhibition Reduces Glucose Levels, Blood Pressure, and Oxidative Stress in Apolipoprotein E Knockout Mice

2017 ◽  
Vol 2017 ◽  
pp. 1-9 ◽  
Author(s):  
Shadi Hamoud ◽  
Rabia Shekh Muhammad ◽  
Niroz Abu-Saleh ◽  
Ahmad Hassan ◽  
Yaniv Zohar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Apolipoprotein E ◽  
Serum Glucose ◽  
The Other ◽  
Control Group ◽  
Glucose Levels ◽  
Disease States ◽  
Apolipoprotein E Knockout Mice ◽  
And Oxidative Stress

Background.Atherosclerosis is a multifactorial process. Emerging evidence highlights a role of the enzyme heparanase in various disease states, including atherosclerosis formation and progression.Objective.The aim of the study was to investigate the effect of heparanase inhibition on blood pressure, blood glucose levels, and oxidative stress in apoE−/− mice.Methods.Male apoE−/− mice were divided into two groups: one treated by the heparanase inhibitor PG545, administered intraperitoneally weekly for seven weeks, and the other serving as control group (injected with saline). Blood pressure was measured a day before sacrificing the animals. Serum glucose levels and lipid profile were measured. Assessment of oxidative stress was performed as well.Results.PG545 significantly lowered blood pressure and serum glucose levels in treated mice. It also caused significant reduction of the serum oxidative stress. For safety concerns, liver enzymes were assessed, and PG545 caused significant elevation only of alanine aminotransferase, but not of the other hepatic enzymes.Conclusion.Heparanase inhibition by PG545 caused marked reduction of blood pressure, serum glucose levels, and oxidative stress in apolipoprotein E deficient mice, possibly via direct favorable metabolic and hemodynamic changes caused by the inhibitor. Possible hepatotoxic and weight wasting effects are subject for future investigation.

Forearm vasoconstriction in response to noradrenaline and NG-monomethyl-L-arginine in essential hypertension

1999 ◽  
Vol 97 (3) ◽  
pp. 277-282 ◽  
Author(s):  
Barry J. KNEALE ◽  
Philip J. CHOWIENCZYK ◽  
Sally E. BRETT ◽  
JohnR. COCKCROFT ◽  
James M. RITTER
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Essential Hypertension ◽  
Forearm Blood Flow ◽  
Venous Occlusion ◽  
Control Group ◽  
No Production ◽  
Primary Role ◽  
Consistent Finding ◽  
And Control

A role for abnormal NO production in essential hypertension remains controversial. Blunted vasoconstriction of forearm resistance vasculature in response to NG-monomethyl-⌊-arginine (⌊-NMMA; an inhibitor of NO biosynthesis), relative to the response to noradrenaline, has been reported in hypertensive patients and interpreted as evidence of reduced basal NO biosynthesis. We sought to determine whether reduced sensitivity of forearm vasculature to the vasoconstrictor action of l-NMMA relative to that of noradrenaline is a consistent finding in essential hypertension. We studied a group of patients (n = 32; blood pressure 176±4/102±2 mmHg; means±S.E.M.) and a group of healthy normotensive controls (n = 32; blood pressure 130±2/75±1 mmHg). Noradrenaline (60–240 pmol·min-1) and ⌊-NMMA (1–4 μmol·min-1) were infused into the brachial artery, and forearm blood flow was measured by venous occlusion plethysmography. The effects of each vasoconstrictor were similar in hypertensive and control subjects. The highest dose of l-NMMA reduced forearm blood flow by 0.75±0.12 ml·min-1·dl-1 in the control group and by 0.89±0.10 ml·min-1·dl-1 in the hypertensive group. The study had 90% power (with P = 0.05) to detect a 10% difference in forearm blood flow response between the hypertensive and control groups. We conclude that reduced sensitivity of forearm resistance vasculature to the vasoconstrictor action of l-NMMA is not a universal feature of essential hypertension. This argues against a primary role for reduced basal NO biosynthesis in skeletal muscle resistance vessels in the pathogenesis of essential hypertension.

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