Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Abdominal aortic coarctation above the renal arteries leads to severe hypertension above the stenotic site and provides a model for simultaneous testing of the effects of increased and decreased pressure and consequently shear stress in the same animal. The effects of increased pressure, per se, on oxidative stress and antioxidant enzyme expression is unknown. We studied the protein expressions of antioxidant enzymes and NADPH oxidase (gp91phox subunit) in the aortic segments above and below the stenosis site in sham-operated control and aortic-banded rats at four weeks postoperatively. Compared with the control group, the banded group showed significant up-regulation of NADPH oxidase, catalase (CAT), Cu/Zn superoxide dismutase (SOD) and Mn SOD protein content in the thoracic aorta. In contrast, Mn SOD, Cu/Zn SOD and NADPH oxidase protein abundance were unchanged in the abdominal aortic segment below the stricture where blood pressure is not elevated, whereas CAT protein abundance was also elevated in the abdominal aorta. No changes were noted for glutathione peroxidase (GPX) protein content either in the thoracic or abdominal aortic segments. Coarctation-induced hypertension is associated with increased aortic CAT, Cu/Zn SOD, Mn SOD and NADPH oxidase protein expression. The up-regulation of NADPH oxidase increases reactive oxygen species (ROS) generation noted in the present study and contributes to inactivation of nitric oxide (NO) as shown previously in this model. Upregulation of antioxidant enzymes may be a compensatory response in the face of elevated pressure and oxidative stress. The normality of protein abundance in the abdominal aorta wherein blood pressure is not elevated points to the role of baromechanical factors, as opposed to circulating humoral factors that were similar in both segments, as a mechanism responsible for increased antioxidant enzyme expression.
 ...
PMID:Effects of aortic coarctation on aortic antioxidant enzymes and NADPH oxidase protein expression. 1558 70

We estimated the nitrate/nitrite, carbonyl groups, reduced glutathione (GSH) and malondialdehyde (MDA) concentrations and Cu,Zn superoxide dismutase (SOD-1), catalase (CAT), glutathione peroxidase (cGSH-Px) and glutathione S-transferase (GST) activities in the blood of 17 normotensive young subjects (mean age 39+/-7.0 years), 21 normotensive elderly subjects (mean age 82+/-8.2 years) and 38 patients with essential arterial hypertension (mean age 73+/-8.0 years). Our examinations showed that hypertension in the elderly is associated with greater than normal levels of protein and lipid oxidation, decreased nitric oxide concentration and an imbalance in antioxidant status (decreased GSH concentration and SOD-1 activity). The increased activity of GST compensated the decreased activity of cGSH-Px in the blood of hypertensive patients. Our study confirms that the degree of oxidative stress in elderly patients intensifies, especially if said patients have associated essential arterial hypertension.
 ...
PMID:The markers of oxidative stress and activity of the antioxidant system in the blood of elderly patients with essential arterial hypertension. 1564 86

Moderate ethanol consumption is known to reduce the risk of cardiovascular diseases; however, chronic high dose ethanol ingestion causes cardiovascular injuries including hypertension. The dose response of ethanol-induced hypertension and associated oxidative stress response has not been well established. This study investigated the dose response of ethanol on blood pressure (BP), nitric oxide (NO) and antioxidants in the plasma of the rat. Male Fisher rats (200-250 g) were divided into five groups of six animals each and treated as follows: (1) control (5% sucrose, orally) daily for 12 weeks; (2) 20-30% ethanol (1 g kg-1, orally) daily for 12 weeks; (3) 20-30% ethanol (2 g kg-1, orally) daily for 12 weeks; (4) 20-30% ethanol (4 g kg-1, orally) daily for 12 weeks; (5) 20-30% ethanol (6 g kg-1, orally) daily for 12 weeks. The BP (systolic, diastolic and mean) was recorded every week through tail-cuff method. The animals were sacrificed 12 weeks after treatments and blood was collected and analyzed. Systolic and mean BP were slightly decreased with 1 g kg-1 dose but significantly elevated with 2, 4 and 6 g kg-1 doses 7-12 weeks after ethanol ingestion. Whereas diastolic BP was significantly elevated with 4 and 6 g kg-1 doses 8-12 weeks after ethanol ingestion. Blood alcohol levels were significantly elevated with 4 and 6 g kg-1 dose of ethanol for 12 weeks. Ethanol dose-dependency increased plasma malondialdehyde (MDA) and protein carbonyl levels, while nitric oxide (NO), ratio of reduced to oxidized glutathione (GSH/GSSG) and antioxidant enzymes: copper/zinc-superoxide dismutase (CuZn-SOD) and manganese (Mn)-SOD, catalase (CAT) and glutathione peroxidase (GSH-Px) activities were decreased 12 weeks post-treatment. The data suggested that ethanol induces hypertension at higher doses by depleting NO and antioxidants and increasing oxidative tissue injury in rats.
 ...
PMID:Dose response of alcohol-induced changes in BP, nitric oxide and antioxidants in rat plasma. 1568 47

Previous studies from this laboratory have demonstrated the presence of oxidative stress and its role in the pathogenesis of lead-induced hypertension. This study was designed to determine whether oxidative stress in animals with lead-induced hypertension is associated with dysregulation of the activities of the main antioxidant enzymes, namely superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX). In addition, we aimed to determine the effect of lead on the regulation of guanylate cyclase (GC) expression. Male Sprague-Dawley rats were randomly assigned to control and lead-exposed groups, and immunodetectable Cu/Zn SOD, Mn SOD, CAT, and GPX were determined by immunoblotting in the thoracic aorta. Additionally, the activities of these enzymes were measured in the renal cortex, medulla, and thoracic aorta. Furthermore, immunodetectable GC was determined in the thoracic aorta. In the thoracic aorta, lead exposure resulted in significant upregulation of aortic Cu/Zn SOD activity, while CAT and GPX activity and CuZn SOD, Mn SOD, and CAT protein abundance were unchanged. Conversely, GC protein abundance was decreased in thoracic aorta. In renal cortex and medulla, CAT and Cu/Zn SOD activities were increased, while GPX activity was unchanged. Lead-exposed animals exhibited upregulation of some antioxidant enzyme activities, most likely as a compensatory response to lead exposure. However, other enzymes did not compensate in the face of oxidative stress, suggestive of an antioxidant/oxidant imbalance. These findings, combined with decrease in aortic GC protein abundance, provide further evidence for dysregulation of antioxidant/oxidant balance and hypertension in this model.
 ...
PMID:Lead-induced dysregulation of superoxide dismutases, catalase, glutathione peroxidase, and guanylate cyclase. 1572 81

In kidney, nitric oxide (NO) produced by nitric oxide synthase (NOS) regulates sodium and water excretion and renal medullary blood flow. However, excessive NO production causes nitrative damage and oxidative stress. Since oxidative stress may be linked to hypertension, we examined the expression and activity of inducible NOS (iNOS) in the kidney of the spontaneously hypertensive rat (SHR) and compared our findings to control normtotensive Wistar Kyoto (WKY) rat. Compared with WKY rat, there was significant (p < .05) overexpression (by 96%) and increased (2-fold) activity of iNOS in the cortex but not in the outer medulla, of SHR kidney; in the inner medulla, there was a 6.9-fold increase in iNOS activity in SHR. Increased expression (by 104%) and activity (3.3-fold) of iNOS was specifically observed in proximal tubules (PTs) of the cortex, accompanied by higher (2-fold) tissue nitrite levels. Although certain antioxidant enzymes such as catalase and Mn-superoxide dismutase were overexpressed, glutathione peroxidase was underexpressed in SHR PTs. Overexpression of the inducer of the iNOS promoter, nuclear factor-kappaB (NF-kappaB), with elevated nitrotyrosinylated proteins, further confirmed an elevated state of iNOS-induced oxidative stress in SHR kidneys, possibly signifying its role in the maintenance of essential hypertension seen in these animals.
 ...
PMID:Overexpression of inducible nitric oxide synthase in the kidney of the spontaneously hypertensive rat. 1577 27

Chronic renal failure (CRF) is associated with oxidative stress, the precise mechanism of which is yet to be elucidated. The present study was undertaken to investigate in renal insufficiency the expression of catalase and glutathione peroxidase, which play a critical role in antioxidant defense system by catalyzing detoxification of hydrogen peroxide (H2O2) and organic hydroperoxides. Rats were randomly assigned to the CRF (5/6 nephrectomized) and sham-operated control groups and observed for 6 weeks. Renal and thoracic aortic catalase and glutathione peroxidase protein abundance was measured by Western blotting. The enzyme activities in the renal and aortic extracts, hepatic glutathione levels, blood pressure and urinary nitric oxide metabolites (NO(x)) excretion were also measured. Blood pressure and urinary nitric oxide metabolite (NO(x)) excretion were also measured. The CRF group showed a significant down-regulation of both immunodetectable catalase and glutathione peroxidase proteins in the remnant kidney. Catalase activity was also significantly decreased in the remnant kidney whereas glutathione peroxidase activity was not significantly affected. Furthermore, the protein abundance of catalase was unchanged whereas the enzyme activity was significantly decreased in the thoracic aorta of CRF animals compared to the sham-operated controls. By contrast, both the protein abundance and the enzyme activity of glutathione peroxidase were not significantly affected in the aorta of CRF animals compared to the sham-operated controls. This was coupled with marked arterial hypertension, significant reduction of hepatic glutathione levels and urinary NO(x) excretion pointing to increased inactivation and sequestration of NO by superoxide. These events point to the role of impaired antioxidant defense system in the pathogenesis of oxidative stress in CRF.
 ...
PMID:Expression of catalase and glutathione peroxidase in renal insufficiency. 1577 43

The aims of the present study were to analyse the effects of an oral daily dose (10 mg/kg) of the dietary flavonoid quercetin for five weeks in two-kidney, one-clip (2K1C) Goldblatt (GB) hypertensive rats. The evolution of systolic blood pressure was followed by weekly measurements, and morphological variables, proteinuria, plasma nitrates plus nitrites (NOx) and thiobarbituric acid reactive substances (TBARS), liver oxidative stress markers and endothelial function were determined at the end of the experimental period. Quercetin treatment reduced systolic blood pressure of GB rats, producing no effect in control animals. It also reduced cardiac hypertrophy and proteinuria developed in GB hypertensive rats. Decreased endothelium-dependent relaxation to acetylcholine of aortic rings from GB rats was improved by chronic quercetin treatment, as well as increased endothelium-dependent vasoconstrictor response to acetylcholine and overproduction of TXB2 by aortic vessels of GB rats, being without effect in normotensive animals. Increased plasma NOx and TBARS, and decreased liver total glutathione (GSH) levels and glutathione peroxidase (GPX) activity were observed in GB hypertensive rats compared to the control animals. Normalisation of plasma NOx and TBARS concentrations and improvement of the antioxidant defences system in liver accompanied the antihypertensive effect of quercetin. We conclude that chronic oral treatment with quercetin shows both antihypertensive and antioxidant effects in this model of renovascular hypertension.
 ...
PMID:Effects of chronic quercetin treatment in experimental renovascular hypertension. 1579 64

Bambusae concretio Salicea (BCS; plant family name: Phyllostachys bambusoides Siebold et Zuccarinii) is a medicinal plant used in Korea for the treatment of various symptoms accompanying hypertension and cerebrovascular disorders. Previously, it was shown that BCS is an effective protectant against oxidative glutamate toxicity in the murine neuroblastoma cells and human neuroblastoma cells. Treatment with BCS increased the secretion of the non-amyloidogenic amyloid precursor protein fragment, and decreased the secretion of amyloid-beta (Abeta) peptides from neuronal cells [Jeong, J.C., Seo, Y.J., Kim, H.M., Lee, Y.C., Kim, C.H., 2003. Inhibitory effects of Bombusae concretio Salicea on neuronal secretion of Alzheimer's beta-amyloid peptides, a neuro-degenerative peptide. Neurochemical Research 28, 1785-1792.]. To further examine the pharmacological activity of BCS, we studied the protective effect of the water extracts on Abeta25-35 peptide-induced neuronal death by microscopic observation and lactate dehydrogenase (LDH) assay, and action on antioxidative enzymes using cultured astrocyte cells. Ten microM Abeta25-35-induced cell death was protected by the application of water extract of BCS in a dose-dependent manner, and concentrations of 1-10 microg/ml had a significant effect compared to exposure to Abeta25-35 only. When antioxidative enzyme activities such as catalase, superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) were assayed after Abeta25-35 treatment, the enzymes were decreased in a similar fashion. However, those activities were enhanced by BCS treatment and this may have resulted from the potentiation of antioxidative ability by BCS. The ability of BCS to reduce cellular cytotoxicity induced by 10 microM Abeta25-35 suggests that BCS may be a protective agent for free radical generating compounds such as Abeta25-35, and that Abeta25-35 is not only a potent lipid peroxide inducer, but also causes changes in antioxidative enzymes. From the results, it was concluded that BCS has a protective effect on Abeta-induced neuronal death in cultured astrocyte cells through the inhibition of lipid peroxidation and protection of antioxidative enzymes.
 ...
PMID:Effects of Bambusae concretio Salicea (Chunchukhwang) on amyloid beta-induced cell toxicity and antioxidative enzymes in cultured rat neuronal astrocytes. 1581 57

The activities of catalase in liver, heart and kidney as well as glutathione peroxidase and superoxide dismutase in liver, heart, kidney, and serum from hypertriglyceridemic and hypertensive female and male rats were measured at 3 and 8 months of daily administration of sucrose in their drinking water. This treatment induces high levels of serum triglycerides, central obesity, moderate hypertension, hyperinsulinemia, and an increase in lipoperoxidation, among other alterations. The experimental periods were chosen on the basis of previous observations: at 3 months the level of serum triglycerides increases significantly above the normal value and remains without major changes thereafter, but the blood pressure only rises significantly at about 4 months in males and 5 months in females. So, at 8 months the rats have been subjected to abnormal conditions for 3-4 months. The effect of these and the influence of sex on levels of antioxidant enzymes were investigated. Both factors, sucrose treatment and sex, were conducive to significant changes in those variables.
 ...
PMID:Activities of antioxidant enzymes in two stages of pathology development in sucrose-fed rats. 1587 Aug 42

This study evaluated the activity of cardiac and renal antioxidant enzymes [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPX), and glutathione reductase (GR)] and whether chronic treatment with tempol, a cell membrane-permeable SOD mimetic, ameliorates the hypertension of hyperthyroidism. Two experiments were performed. In experiment I, the following four groups of male Wistar rats were used: control group and three groups that received thyroxine (T4) at 10, 50, or 75 microg x rat(-1) x day(-1). In experiment II, tempol was orally administered (18 mg x kg(-1) x day(-1)) to control and T4-treated (75 microg x rat(-1) x day(-1)) rats. All treatments were maintained for 6 wk. Body weight, tail systolic blood pressure (BP), and heart rate were measured one time a week, and direct BP and morphological, metabolic, plasma, and renal variables were measured at the end of the experiment. Enzymatic activities were measured in renal cortex and medulla and right and left ventricles. In renal cortex, SOD activity was decreased in the T4-75 group, and there was a dose-related increase in CAT activity and decrease in GPX and GR activities in T4-treated groups. Activity of all antioxidant enzymes was reduced in left ventricle in T4-50 and T4-75 groups and in right ventricle in the T4-75 group. Tempol reduced BP, plasma malondialdehyde, and total urinary excretion of F2 isoprostanes in hypertensive hyperthyroid rats but not in controls. Tempol did not improve cardiac hypertrophy, proteinuria, or creatinine clearance in hyperthyroid rats. In conclusion, the results obtained indicate that the activity of SOD, GPX, and GR in renal and cardiac tissues is decreased in hyperthyroidism and that antioxidant treatment with tempol ameliorates T4-induced hypertension.
 ...
PMID:Cardiac and renal antioxidant enzymes and effects of tempol in hyperthyroid rats. 1594 80


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>