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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxidative stress plays an important role in arterial hypertension and propionyl-L-carnitine (PLC) has been found to protect cells from toxic reactive oxygen species. In this work, we have evaluated the antioxidant capacity of chronic PLC treatment in spontaneously hypertensive rats (SHR) by measuring the activity of antioxidant enzymes and the lipid peroxidation in liver and cardiac tissues. The activity of glutathione peroxidase was decreased in liver and cardiac tissues of SHR when compared with their normotensive controls, Wistar- Kyoto (WKY) rats, this alteration being prevented by PLC treatment. Glutathione reductase activity was increased in hypertensive rats and no effect was observed after the treatment. No significant changes in superoxide dismutase activity were observed among all experimental groups. Liver of hypertensive rats showed higher catalase activity than that of normotensive rats, and PLC enhanced this activity in both rat strains. Thiobarbituric acid reactive substances, determined as a measure of lipid peroxidation, were increased in SHR compared with WKY rats, and PLC treatment decreased these values not only in hypertensive rats but also in normotensive ones. The content of carnitine in serum, liver and heart was higher in PLC-treated rats, but PLC did not prevent the hypertension development in young SHR. In addition, triglyceride levels, which were lower in SHR than WKY rats, were reduced by chronic PLC treatment in both rat strains. These results demonstrate: i) the hypotriglyceridemic effect of PLC and ii) the antioxidant capacity of PLC in SHR and its beneficial use protecting tissues from hypertension-accompanying oxidative damage.
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PMID:Antioxidant activity of propionyl-L-carnitine in liver and heart of spontaneously hypertensive rats. 1626 37

Free radicals and associated oxidative stress induced by alloxan are implicated in eliciting pathological changes in diabetes mellitus. Terminalia arjuna bark, an indigenous plant used in ayurvedic medicine in India, primarily as a cardiotonic is also used in treating diabetes, anemia, tumors and hypertension. The present study examined the effect of ethanolic extract (250 and 500 mg/kg body weight) of Terminalia arjuna stem bark in alloxan induced diabetic rats and its lipid peroxidation, enzymatic and nonenzymatic activity was investigated in the liver and kidney tissues. The extract produced significant (P<0.05) reduction in lipid peroxidation (LPO). The effect of oral T. arjuna at the dose of 500 mg/kg body weight was more than the 250 mg/kg body weight. The extract also causes a significant (P<0.05) increase in superoxide dismutase, catalase, glutathione peroxidase, glutathione-s-transferase glutathione reductase and glucose-6-phosphate dehydrogenase, reduced glutathione, vitamin A, vitamin C, vitamin E, total sulfhydryl groups (TSH) and non protein sulfhydryl groups (NPSH) in liver and kidney of alloxan induced diabetic rats, which clearly shows, the antioxidant property of T. arjuna bark. The result indicates that the extract exhibit the antioxidant activity through correction of oxidative stress and validates the traditional use of this plant in diabetic animals.
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PMID:Effect of Terminalia arjuna stem bark on antioxidant status in liver and kidney of alloxan diabetic rats. 1705 32

The present study aimed to investigate whether l-carnitine (LC) protects the vascular endothelium and tissues against oxidative damage in hypertension. Antioxidant enzyme activities, glutathione and lipid peroxidation were measured in the liver and heart of spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats. Nitrite and nitrate levels and total antioxidant status (TAS) were evaluated in plasma, and the expression of endothelial nitric oxide synthase (eNOS) and p22phox subunit of NAD(P)H oxidase was determined in aorta. Glutathione peroxidase activity was lower in SHR than in WKY rats, and LC increased this activity in SHR up to values close to those observed in normotensive animals. Glutathione reductase and catalase activities, which were higher in SHR, tended to increase after LC treatment. No differences were found in the activity of superoxide dismutase among any animal group. The ratio between reduced and oxidized glutathione and the levels of lipid peroxidation were respectively decreased and increased in hypertensive rats, and both parameters were normalized after the treatment. Similarly, LC was able to reverse the reduced plasma nitrite and nitrate levels and TAS observed in SHR. We found no alterations in the expression of aortic eNOS among any group; however, p22phox mRNA levels showed an increase in SHR that was reversed by LC. In conclusion, chronic administration of LC leads to an increase in hepatic and cardiac antioxidant defense and a reduction in the systemic oxidative process in SHR. Therefore, LC might increase NO availability in SHR aorta by a reduction in superoxide anion production.
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PMID:L-carnitine attenuates oxidative stress in hypertensive rats. 1714 29

Oxidative stress may initiate significant hepatocyte injury in subjects with fatty liver. We characterized changes in hepatic oxidative anti-oxidative parameters in rats given a fructose-enriched diet (FED) with and without medications to reduce blood pressure or plasma triglycerides. FED rats had an increase in malondialdehyde (MDA) concentration, a reduction in alpha-tocopherol concentration, a reduction in paraoxonase (PON) activity, an increase in glutathione peroxidase (GSH-Px), and glutathione reductase (GSSG-R) activity. Amlodipine increased PON and GSH-Px, but decreased GSSG-R activity and alpha-tocopherol concentration. Captopril decreased MDA concentration and the activity of both GSH-Px and GSSG-R, but increased alpha-tocopherol concentration and PON activity. Bezafibrate increased alpha-tocopherol concentration and PON activity, but decreased the activity of GSSG-R. Animals with fatty liver exhibit an increase in peroxidative stress but also a defect in anti-oxidative pathways. Drugs administered to treat hypertension and hypertriglyceridemia could lead to a variety of changes in the hepatic oxidative, anti-oxidative milieu.
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PMID:Effects of amlodipine, captopril, and bezafibrate on oxidative milieu in rats with fatty liver. 1771 May 47

We evaluated whether the blockade of the proinflammatory transcription factor NF-kappaB would modify the oxidative stress, inflammation, and structural and hemodynamic alterations found in the kidney as a result of massive proteinuria. Twenty male Sprague-Dawley rats were injected with 2 g of BSA intraperitoneally daily for 2 wk. Ten of them received in addition the inhibitor of NF-kappaB activation pyrrolidine dithiocarbamate (PDTC; 200 mg.kg(-1).day(-1) sc) and the rest received vehicle. Seven rats that received intraperitoneal saline were used as controls. Glomerular hemodynamics were studied after 14 days. Markers of oxidative stress (NF-kappaB subunit p65+ cells, 3-nitrotyrosine, and 4-hydroxynonenal), inflammation (cortical CD68+ cells and NOS-II), and afferent arteriole damage were assessed by immunohistochemistry and morphometry. Activity of antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase was evaluated in renal cortex and medulla. Albumin overload induced massive proteinuria, oxidative stress with reduced activity of antioxidant enzymes, NF-kappaB activation, inflammatory cell infiltration, a significant presence of proteinaceous casts, systemic and glomerular hypertension, as well as arteriolar remodeling. Treatment with PDTC prevented or improved all of these findings. In this model of nephrotic syndrome, we demonstrate a key role for oxidative stress and inflammation in causing systemic and glomerular hypertension and proteinuria. Oxidative stress and inflammation may have a key role in accelerating renal injury associated with intense proteinuria.
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PMID:Treatment with pyrrolidine dithiocarbamate improves proteinuria, oxidative stress, and glomerular hypertension in overload proteinuria. 1875 1

Congenital malformations of neonates are one of the adverse effects of diabetic pregnancy which can be prevented by supplementation of vitamin E and C. The survived neonates usually are at higher risk to diabetes, hypertension, dyslipidemia and cardiovascular diseases that may possibly be prevented through antioxidants administration. In view of this information, the efficacy of modified poultry egg enriched with optimum minerals, vitamin E and omega-3 fatty acids was studied on F1-generation, which were made to survive by feeding them this modified egg to diabetic mothers of Wistar rats. The survived F1-generation displayed hyperglycemia, dyslipidemia and hypertension like their parents, evaluated after three months of the experiment. Their mineral status revealed a higher Zn and lower Cu, Mg and Mn levels in liver and kidney. Their lipid peroxidation products were however higher and the enzyme activities of superoxide dismutase, catalase, glutathione-S-transferase, glutathione reductase, glutathione (reduced) and glucose -6 phosphate dehydrogenase were significantly lower. In the other group of F1-generation, fed modified egg mixed diet, a significant reduction in the blood pressure, serum glucose, serum lipid profile, and the lipid peroxidation products, and a significant increase in the activities of enzymes per se with reversal of Zn, Cu, Mg and Mn levels closer to the control group were recorded. The data suggest that the modified egg can ameliorate the oxidative stress in F1-generation of diabetic rats by improving the mineral status in their body.
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PMID:Beneficial effects of modified egg* on oxidative stress in F1- generation of metabolic syndrome-X induced Wistar rat. 1937 65

Preeclampsia is characterized by vascular endothelial dysfunction partly attributed to oxidative stress. In the vasculature of preeclamptic women, we have shown increased lectin-like oxidized low-density lipoprotein receptor 1 (LOX-1) and arginase expression, which can contribute to vascular oxidative stress. However, the mechanisms of such upregulation are unknown. Methylglyoxal (MG) that plays a role in the vascular complications of diabetes mellitus and the development of hypertension can be one potential factor that can affect LOX-1 and arginase through its ability to induce oxidative stress in vascular cells. MG also reacts with lysine residues in proteins to generate advanced glycation end product, N(epsilon)-carboxy ethyl lysine, which also serves as a marker of MG. We hypothesized that markers of MG formation will be increased in the vasculature of preeclamptic women and that exogenous MG will induce oxidative stress by the upregulation of LOX-1 via arginase. We observed increased N(epsilon)-carboxy ethyl lysine expression in the vasculature of women with preeclampsia in comparison with normotensive pregnant women. Moreover, glyoxalase I and II, enzymes that detoxify MG, and glutathione reductase, which generates reduced glutathione, a cofactor for glyoxalase, are also reduced in preeclampsia. In cultured endothelial cells, MG increased arginase expression by 6 hours and LOX-1 expression by 24 hours. Inhibition of arginase or NO synthase significantly reduced MG-induced LOX-1 expression, superoxide levels, and nitrotyrosine staining. In conclusion, MG-induced LOX-1 expression is mediated via arginase upregulation likely because of uncoupling of NO synthase, which may have implications in preeclampsia.
Hypertension 2009 Oct
PMID:Evidence for increased methylglyoxal in the vasculature of women with preeclampsia: role in upregulation of LOX-1 and arginase. 1968 46

Angiotensin-converting enzyme inhibitors are effective at reducing blood pressure, whereas statins decrease plasma cholesterol impeding atherosclerosis. It is hypothesized that these medications may improve blood pressure and serum cholesterol by modifying the antioxidative status and energy metabolism of erythrocytes. In this study, the effects of 2 treatments are compared: lisinopril alone versus lisinopril + simvastatin, on erythrocyte antioxidant and energy metabolic enzymes. Patients with atherosclerosis and moderate hypertension are randomly assigned to receive lisinopril 10 to 20 mg/d or lisinopril 10 to 20 mg/d plus simvastatin 20 mg/d for 24 weeks. Higher catalase activity and lower glutathione peroxidase activity are observed in 94% to 100% patients from both groups after 12 and 24 weeks of treatment. Superoxide dismutase activity is increased significantly only after 24 weeks. No changes of glutathione reductase, lactate dehydrogenase, and phosphofructokinase activities are found under any conditions indicated. Both treatments decrease systolic and diastolic blood pressure equally. Only lisinopril + simvastatin treatment decreases plasma total cholesterol and low-density lipoprotein cholesterol. The results show for the first time that lisinopril monotherapy and combined lisinopril + simvastatin therapy exhibit specific and pronounced effects on antioxidant and energy metabolic enzyme activities in erythrocytes of hypertensive patients.
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PMID:Specific and pronounced impacts of lisinopril and lisinopril plus simvastatin on erythrocyte antioxidant enzymes. 1984 Nov 60

Acute subcutaneous administration of Angiotensin II (Ang II) causes a rise in blood pressure in diabetic Wistar rats. Diabetes was induced using streptozotocin (70 mg/kg, i.v.). Chronic administration of pomegranate juice (PJ) extract (100 mg/kg and 300 mg/kg; p.o. for 4 weeks) obtained from Punica granatum (punicaceae) fruits reduced the mean arterial blood pressure and vascular reactivity changes to various catecholamines and also reversed the biochemical changes induced by diabetes and Ang II. PJ treatment also caused a significant decrease in levels of thiobarbituric acid reactive substances (TBARS) in kidney and pancreas while activities of enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione reductase (GSH) showed significant elevation. The cumulative concentration response curve (CCRC) of Ang II was shifted towards right in rats treated with PJ using isolated strip of ascending colon. In histopathological examination, PJ treatment prevented the tubular degenerative changes induced by diabetes. The results suggest that the PJ extract could prevent the development of high blood pressure induced by Ang II in diabetic rats probably by combating the oxidative stress induced by diabetes and Ang II and by inhibiting ACE activity. In conclusion, PJ has antihypertensive action in Ang II diabetic model.
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PMID:Effect of pomegranate juice on Angiotensin II-induced hypertension in diabetic Wistar rats. 2002 May 14

It has been shown that oxidative stress is involved in the pathogenesis of arterial hypertension. The aim of this work was to study and compare the molecular mechanisms of the antioxidant properties of l-carnitine and captopril in spontaneously hypertensive rats (SHR). Antioxidant enzyme activity/regulation (glutathione peroxidase, glutathione reductase and superoxide dismutase) was measured in the erythrocytes and hearts of SHR. The molecular expression of endothelial nitric oxide synthase (eNOS), NADPH oxidase, angiotensin converting enzyme (ACE), angiotensin II type I receptor (AT(1) receptor) and NF-kappaB/IkappaB system was also measured in the hearts of these animals. Both l-carnitine and captopril augmented the antioxidant defense capacity in SHRs. This effect was mediated by an upregulation of antioxidant enzymes, an increase in the plasma total antioxidant capacity and a reduction of lipid peroxidation and superoxide anion production in the heart. The administration of both compounds to hypertensive animals also produced an upregulation of eNOS and a normalization of ACE, angiotensin AT(1) receptor, and the NF-kappaB/IkappaB system expression. In addition, captopril reduced the arterial blood pressure and the relative heart weights back to control values, whereas l-carnitine caused only a partial reduction of blood pressure values and did not alter the cardiac hypertrophy found in SHRs. In conclusion, we have found that l-carnitine and captopril have a similar antioxidant effect in the hearts of hypertensive rats. The molecular regulation of antioxidant enzymes through an inhibition of the renin-angiotensin system and a modulation of the NF-kappaB/IkappaB system seems to be responsible for this antioxidant effect.
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PMID:Comparative effects of captopril and l-carnitine on blood pressure and antioxidant enzyme gene expression in the heart of spontaneously hypertensive rats. 2012 95


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