scholarly journals Clinical and Experimental Evidences of Hydrogen Sulfide Involvement in Lead-Induced Hypertension

2018 ◽  
Vol 2018 ◽  
pp. 1-13 ◽  
Author(s):  
José Sérgio Possomato-Vieira ◽  
Victor Hugo Gonçalves-Rizzi ◽  
Regina Aparecida do Nascimento ◽  
Rodrigo Roldão Wandekin ◽  
Mayara Caldeira-Dias ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Hydrogen Sulfide ◽  
Cardiovascular Effects ◽  
Blood Lead ◽  
Rat Aorta ◽  
Protective Role ◽  
Sodium Hydrosulfide ◽  
Induced Hypertension ◽  
Male Wistar Rats

Lead- (Pb-) induced hypertension has been shown in humans and experimental animals and cardiovascular effects of hydrogen sulfide (H2S) have been reported previously. However, no studies examined involvement of H2S in Pb-induced hypertension. We found increases in diastolic blood pressure and mean blood pressure in Pb-intoxicated humans followed by diminished H2S plasmatic levels. In order to expand our findings, male Wistar rats were divided into four groups: Saline, Pb, NaHS, and Pb + NaHS. Pb-intoxicated animals received intraperitoneally (i.p.) 1st dose of 8 μg/100 g of Pb acetate and subsequent doses of 0.1 μg/100 g for seven days and sodium hydrosulfide- (NaHS-) treated animals received i.p. NaHS injections (50 μmol/kg/twice daily) for seven days. NaHS treatment blunted increases in systolic blood pressure, increased H2S plasmatic levels, and diminished whole-blood lead levels. Treatment with NaHS in Pb-induced hypertension seems to induce a protective role in rat aorta which is dependent on endothelium and seems to promote non-NO-mediated relaxation. Pb-intoxication increased oxidative stress in rats, while treatment with NaHS blunted increases in plasmatic MDA levels and increased antioxidant status of plasma. Therefore, H2S pathway may be involved in Pb-induced hypertension and treatment with NaHS exerts antihypertensive effect, promotes non-NO-mediated relaxation, and decreases oxidative stress in rats with Pb-induced hypertension.

scholarly journals Antioxidant Effects of Bovine Lactoferrin on Dexamethasone-Induced Hypertension in Rat

2014 ◽  
Vol 2014 ◽  
pp. 1-6 ◽  
Author(s):  
Leila Safaeian ◽  
Hadi Zabolian
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Body Weight Loss ◽  
Chronic Administration ◽  
Bovine Lactoferrin ◽  
Antioxidant Power ◽  
Body Weights ◽  
Induced Hypertension ◽  
Male Wistar Rats ◽  
Ferric Reducing Antioxidant Power

Dexamethasone- (Dex-) induced hypertension is associated with enhanced oxidative stress. Lactoferrin (LF) is an iron-binding glycoprotein with antihypertensive properties. In this study, we investigated the effect of chronic administration of LF on oxidative stress and hypertension upon Dex administration. Male Wistar rats were treated by Dex (30 μg/kg/day subcutaneously) or saline for 14 days. Oral bovine LF (30, 100, 300 mg/kg) was given from day 8 to 14 in a reversal study. In a prevention study, rats received 4 days of LF treatment followed by Dex and continued during the test period. Systolic blood pressure (SBP) was measured using tail-cuff method. Thymus weight was used as a marker of glucocorticoid activity. Plasma hydrogen peroxide (H2O2) concentration and ferric reducing antioxidant power (FRAP) value were determined. Dexamethasone significantly increased SBP and plasma H2O2 level and decreased thymus and body weights. LF lowered (P<0.01) and dose dependently prevented (P<0.001) Dex-induced hypertension. LF prevented body weight loss and significantly reduced the elevated plasma H2O2 and increased FRAP values. Chronic administration of LF strongly reduced the blood pressure and production of ROS and improved antioxidant capacity in Dex-induced hypertension, suggesting the role of inhibition of oxidative stress as another mechanism of antihypertensive action of LF.

scholarly journals Regulation of Biogenesis and Fusion/Fission Processes of Vascular Mitochondria In Aldosterone-Induced Hypertension

2018 ◽  
Vol 10 (1) ◽  
pp. 76-85
Author(s):  
Elena Olivares-Álvaro ◽  
María Belén Ruiz-Roso ◽  
Mercedes Klett-Mingo ◽  
Sandra Ballesteros ◽  
Ricardo Gredilla ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Protein Expression ◽  
Mitochondrial Biogenesis ◽  
Wistar Rats ◽  
Mitochondrial Alterations ◽  
Induced Hypertension ◽  
Male Wistar Rats ◽  
Vascular Oxidative Stress

Background:Aldosterone plays a key role in the development of endothelial dysfunction and hypertension. The regulation of biogenesis and fusion/fission processes of vascular mitochondria has not been examined in aldosterone-induced hypertension. Thereby, we sought to explore in greater depth the role of aldosterone in mitochondrial biogenesis and fusion/fission processes in hypertension and the associated increases in oxidative stress.Methods:Male Wistar rats received aldosterone (1mg/Kg/day) + 1% NaCl as drinking water for 3 weeks.Results:Systolic blood pressure was elevated (p<0.05) in aldosterone-treated rats. eNOS and p-eNOSSer1177protein expression was down regulated (p<0.05) and NADPH oxidase subunit p22phox expression was increased (p<0.05) in aldosterone-treated rats. Expression of mitochondrial biogenesis proteins SIRT1, PGC1α, PPARγ, and TFAM decreased (p<0.05) in aldosterone-treated rats. Protein expression of vascular DRP1, OMA1 and S-OPA1 up regulated (p<0.05) in aldosterone-treated rats. MFN1 and L-OPA1 (p<0.05) decreased in aldosterone-treated animals.Conclusion:The results showed that, in aldosterone-treated rats, hypertension is likely associated with increased oxidative stress in the aorta and with changes in the regulation of two key mitochondrial processes such as biogenesis and fusion/fission processes. The overall mitochondrial alterations observed in the study may play a role in aldosterone-derived vascular oxidative stress and hypertension.

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 In Vivo Antioxidant And Kidney Protective Potential Of Atorvastatin In Rat Cadmium-Induced Toxicity

2021 ◽  
Author(s):  
Esmaeil Karami ◽  
Zahra Goodarzi ◽  
Ali Ghanbari ◽  
Ahmad Reza Bandegi ◽  
Sedighe Yosefi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Biochemical Parameters ◽  
Cadmium Chloride ◽  
Rat Kidney ◽  
Intraperitoneal Administration ◽  
Kidney Injury ◽  
Protective Role ◽  
Histological Changes ◽  
Male Wistar Rats

Abstract Purpose: Environmental and occupational exposure to cadmium chloride is known to cause nephrotoxicity linked with oxidative stress in humans and animals. This study used Atorvastatin to examine its effect on cadmium chloride-induced nephrotoxicity in rat model using biochemical and histological methodologies.Methods: Experiments were performed on 56 adult male Wistar rats (200 ±20 g), randomly assigned to eight groups. Atorvastatin was administered by oral for 15 days at 20 mg/kg/day, started 7 days before cadmium chloride intraperitoneal administration (1, 2, and 3 mg/kg) for eight days. On day 16, blood samples were collected, and kidneys were excised to evaluate the biochemical and histopathological changes.Cadmium chloride significantly increased malondialdehyde (MDA), serum creatinine (Cr), blood urea nitrogen (BUN), and decreased superoxide dismutase (SOD), glutathione (GSH), and glutathione peroxidase (GPx) levels. Results: Administration of Atorvastatin (20 mg/kg) significantly improved lipid peroxidation, glutathione and activities of antioxidant enzymes and significantly decreased BUN and Creatinine. Atorvastatin clearly improved the histological changes, demonstrating its protective role against Cadmium chloride-induced kidney injury.Conclusion: Treatment with Atorvastatin significantly improves all biochemical parameters and suggests a protecting role against cadmium chloride-induced oxidative stress and histological changes in rat kidney.

Mechanical and Dimensional Adaptation of Rat Aorta to Hypertension

1994 ◽  
Vol 116 (3) ◽  
pp. 278-283 ◽  
Author(s):  
T. Matsumoto ◽  
K. Hayashi
Keyword(s):  
Blood Pressure ◽  
Elastic Modulus ◽  
Wall Stress ◽  
Dimensional Change ◽  
Biological Tissues ◽  
Rat Aorta ◽  
Mechanical Adaptation ◽  
Male Wistar Rats ◽  
Load Effects

To investigate mechanisms of the mechanical adaptation of soft biological tissues to load, effects of hypertension on the mechanical properties and wall dimensions of thoracic aortas were studied in rats. Goldblatt hypertension was induced in male Wistar rats aged 8 to 9 weeks by constricting their left renal arteries. Two, 4, 8, or 16 weeks after the operation, thoracic aortas were excised and used to determine static pressure-diameter relations and wall dimensions. Wall thickness correlated significantly with the systolic blood pressure before sacrifice, Psys, at each period. The aortic hoop stress became almost constant at all Psys 2 weeks after the operation. On the other hand, the stress calculated for 100 and 200 mmHg correlated negatively with Psys. The incremental elastic modulus of the wall at Psys had a significant correlation with Psys having a positive slope at each period, although the correlation disappeared at 16 weeks after the operation. These results imply that: 1) thickness of the aortic wall increases very rapidly in response to hypertension; 2) wall stress developed by the in-situ blood pressure is kept constant at a normal level irrespective of hypertension; 3) elastic modulus of the wall of the hypertensive rats at the in-situ blood pressure becomes equal to the normal value after relatively long period of time; 4) in response to the alteration of the applied force, dimensional change appears much earlier than the change in the elastic properties.

scholarly journals The Protective Role of Hydrogen Sulfide Against Obesity-Associated Cellular Stress in Blood Glucose Regulation

Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1038
Author(s):  
Ania Mezouari ◽  
Radhika Nangia ◽  
Jeffrey Gagnon
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Blood Glucose ◽  
Cell Function ◽  
Fasting Blood Glucose ◽  
Protective Role ◽  
Oral Glucose ◽  
Chow Diet ◽  
L Cells ◽  
L Cell

Circulating palmitic acid (PA) is increased in obesity and causes metabolic stress, leading to diabetes. This includes the impairment of the glucoregulatory hormone glucagon-like peptide-1 (GLP-1) secreted from intestinal L-cells. Recently, the anti-inflammatory gasotransmitter hydrogen sulfide (H2S) has been implicated in the enhancement of GLP-1 secretion. We hypothesized that H2S can reduce the oxidative stress caused by palmitate and play a protective role in L-cell function. This study was conducted on both human and mouse L-cells and a mouse model of Western diet (WD)-induced obesity. PA-induced L-cell stress was assessed using DCF-DA. H2S was delivered using the donor GYY4137. C57BL/6 mice were fed either chow diet or PA-enriched WD for 20 weeks with ongoing measurements of glycemia and GLP-1 secretion. In both L-cell models, we demonstrated that PA caused an increase in reactive oxygen species (ROS). This ROS induction was partially blocked by the H2S administration. In mice, the WD elevated body weight in both sexes and elevated fasting blood glucose and lipid peroxidation in males. Additionally, a single GYY4137 injection improved oral glucose tolerance in WD-fed male mice and also enhanced glucose-stimulated GLP-1 release. To conclude, H2S reduces oxidative stress in GLP-1 cells and can improve glucose clearance in mice.

Dietary linoleic acid and salt-induced hypertension

1981 ◽  
Vol 59 (8) ◽  
pp. 872-875 ◽  
Author(s):  
Murray C. Macdonald ◽  
Robert L. Kline ◽  
Gordon J. Mogenson
Keyword(s):  
Blood Pressure ◽  
Linoleic Acid ◽  
Systolic Blood Pressure ◽  
Wistar Rats ◽  
Sodium Content ◽  
Significant Elevation ◽  
Dietary Linoleic Acid ◽  
Low Level ◽  
Induced Hypertension ◽  
Male Wistar Rats

Male Wistar rats chronically fed a low level (0.41%) of linoleic acid (LA) in the diet as supplied by 5% olive oil developed a significant elevation of systolic blood pressure as compared with rats fed either a medium (4.2%) or high (9.4%) level of dietary LA. Chronic excess intake of NaCl (3.75% in the diet) was associated with a significant elevation of blood pressure on all three diets but a low level of LA in the diet exaggerated the salt-induced hypertension. The results suggest that inadequate dietary LA may result in an increase in systolic blood pressure regardless of the sodium content of the diet.

scholarly journals Effects of Clofibrate on Salt Loading-Induced Hypertension in Rats

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Antonio Cruz ◽  
Isabel Rodríguez-Gómez ◽  
Rocío Pérez-Abud ◽  
Miguel Ángel Vargas ◽  
Rosemary Wangensteen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Thyroid Hormone ◽  
Wistar Rats ◽  
Sodium Balance ◽  
Salt Loading ◽  
Blood Pressure Elevation ◽  
Hormone Levels ◽  
Induced Hypertension ◽  
Male Wistar Rats ◽  
Thyroid Hormone Levels

The effects of clofibrate on the hemodynamic and renal manifestations of increased saline intake were analyzed. Four groups of male Wistar rats were treated for five weeks: control, clofibrate (240 mg/kg/day), salt (2% via drinking water), andsalt+clofibrate. Body weight, systolic blood pressure (SBP), and heart rate (HR) were recorded weekly. Finally, SBP, HR, and morphologic, metabolic, plasma, and renal variables were measured. Salt increased SBP, HR, urinary isoprostanes, NOx, ET, vasopressin and proteinuria and reduced plasma freeT4(FT4) and tissueFT4andFT3versus control rats. Clofibrate prevented the increase in SBP produced by salt administration, reduced the sodium balance, and further reduced plasma and tissue thyroid hormone levels. However, clofibrate did not modify the relative cardiac mass, NOx, urinary ET, and vasopressin of saline-loaded rats. In conclusion, chronic clofibrate administration prevented the blood pressure elevation of salt-loaded rats by decreasing sodium balance and reducing thyroid hormone levels.

scholarly journals The Cardiovascular Effects of Central Hydrogen Sulfide Are Related to KATP Channels Activation

2011 ◽  
pp. 729-738 ◽  
Author(s):  
W.-Q. LIU ◽  
C. CHAI ◽  
X.-Y. LI ◽  
W.-J. YUAN ◽  
W.-Z. WANG ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Hydrogen Sulfide ◽  
Katp Channel ◽  
Channel Blocker ◽  
Cardiovascular Effects ◽  
Katp Channels ◽  
Channel Activation ◽  
The Central Nervous System ◽  
Dose Dependent Decrease ◽  
Dose Dependent

Hydrogen sulfide (H2S), an endogenous “gasotransmitter”, exists in the central nervous system. However, the central cardiovascular effects of endogenous H2S are not fully determined. The present study was designed to investigate the central cardiovascular effects and its possible mechanism in anesthetized rats. Intracerebroventricular (icv) injection of NaHS (0.17~17 μg) produced a significant and dose-dependent decrease in blood pressure (BP) and heart rate (HR) (P<0.05) compared to control. The higher dose of NaHS (17 μg, n=6) decreased BP and HR quickly of rats and 2 of them died of respiratory paralyse. Icv injection of the cystathionine beta-synthetase (CBS) activator s-adenosyl-L-methionine (SAM, 26 μg) also produced a significant hypotension and bradycardia, which were similar to the results of icv injection of NaHS. Furthermore, the hypotension and bradycardia induced by icv NaHS were effectively attenuated by pretreatment with the KATP channel blocker glibenclamide but not with the CBS inhibitor hydroxylamine. The present study suggests that icv injection of NaHS produces hypotension and bradycardia, which is dependent on the KATP channel activation.

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