Superoxide dismutase and oxidative stress in Dahl salt-sensitive and -resistant rats

Meng, Shumei; Roberts, L. Jackson; Cason, Garrick W.; Curry, Travis S.; Manning, R. Davis

doi:10.1152/ajpregu.00346.2001

Cited by 133 publications

(152 citation statements)

References 31 publications

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“…Salt loading increases the excretion of isoprostanes in the hypertensive Dahl salt-sensitive rat (7). It is interesting that in Figure 1.…”

Section: Discussionmentioning

confidence: 91%

“…ROS activate mitogen-activated protein kinase in renal tubule cells (38), contribute to hypertrophic responses to Ang II (38) and to cellular injury (39), and increase fibrogenic matrix protein synthesis in mesangial cells (40). A high salt intake enhances oxidative stress in rat skeletal muscle arterioles and vessels (23) and increases BP, protein excretion, and renal fibrosis and worsens renal function in several models of chronic renal failure (7,38,(41)(42)(43) and accelerates the decline of renal function in patients with chronic renal failure (44). Conversely, salt restriction ameliorates renal disease progression in animal models (42) and is recommended for patients with chronic renal failure (45).…”

Section: Discussionmentioning

confidence: 99%

“…Oxidative stress has been implicated in many forms of angiotensin II (Ang II)-related hypertension (1)(2)(3). However, there is also substantial oxidative stress in the tissues or blood vessels of rats with desoxycorticosterone acetate-salt hypertension in which the circulating renin-angiotensin-aldosterone system is suppressed profoundly (4,5) and in models of salt-sensitive hypertension (6,7) and in normal rats fed a high-salt diet (8). Oxidative stress in hypertension has been demonstrated by the increased production of markers, such on the lipid peroxidation products isoprostanes (9) and malonyldialdehyde (MDA), and by BP lowering effects of cell-permeable forms of SOD (10) or its mimetics (9).…”

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confidence: 99%

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Salt Intake, Oxidative Stress, and Renal Expression of NADPH Oxidase and Superoxide Dismutase

Kitiyakara

Chabrashvili²,

Chen³

et al. 2003

Journal of the American Society of Nephrology

281

236

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Abstract. The hypothesis that a high salt (HS) intake increases oxidative stress was investigated and was related to renal cortical expression of NAD(P)H oxidase and superoxide dismutase (SOD). 8-Isoprostane PGF 2␣ and malonyldialdehyde were measured in groups (n ϭ 6 to 8) of conscious rats during low-salt, normal-salt, or HS diets. NADPH-and NADH-stimulated superoxide anion (O 2 ·Ϫ ) generation was assessed by chemiluminescence, and expression of NAD(P)H oxidase and SOD were assessed with real-time PCR. Excretion of 8-isoprostane and malonyldialdehyde increased incrementally twoto threefold with salt intake (P Ͻ 0.001), whereas prostaglandin E 2 was unchanged. Renal cortical NADH-and NADPHstimulable O 2 ·Ϫ generation increased (P Ͻ 0.05) 30 to 40% with salt intake. Compared with low-salt diet, HS significantly (P Ͻ 0.005) increased renal cortical mRNA expression of gp91 phox and p47 phox and decreased expression of intracellular CuZn (IC)-SOD and mitochondrial (Mn)-SOD. Despite suppression of the renin-angiotensin system, salt loading enhances oxidative stress. This is accompanied by increased renal cortical NADH and NADPH oxidase activity and increased expression of gp91 phox and p47 phox and decreased IC-and Mn-SOD. Thus, salt intake enhances generation of O 2 ·Ϫ accompanied by enhanced renal expression and activity of NAD(P)H oxidase with diminished renal expression of IC-and Mn-SOD.

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“…Salt loading increases the excretion of isoprostanes in the hypertensive Dahl salt-sensitive rat (7). It is interesting that in Figure 1.…”

Section: Discussionmentioning

confidence: 91%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

See 1 more Smart Citation

Salt Intake, Oxidative Stress, and Renal Expression of NADPH Oxidase and Superoxide Dismutase

Kitiyakara

Chabrashvili²,

Chen³

et al. 2003

Journal of the American Society of Nephrology

281

236

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show abstract

“…[2][3][4] Increased activity of the NAD(P)H oxidase system is expected to be associated with reduced NO levels, vascular dysfunction, hypertension and salt sensitivity. [4][5][6] The latter, is known to be associated with reduced NO bioactivity [7][8][9][10][11][12][13] and increased superoxide production. 5,6 Consequently, genetic and/or disease-induced changes in NADPH oxidase activity and superoxide formation may play an important role in the pathogenesis of saltsensitive hypertension.…”

Section: Introductionmentioning

confidence: 99%

NAD(P)H oxidase p22phox gene C242T polymorphism, nitric oxide production, salt sensitivity and cardiovascular risk factors in Hispanics

et al. 2006

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Mutations in the NAD(P)H oxidase gene may be associated with abnormal superoxide generation, nitric oxide (NO) availability and cardiovascular diseases. We investigated the prevalence of the NAD(P)H oxidase p22phox gene C242T polymorphism, and its possible association with blood pressure, NO production, salt sensitivity and cardiovascular risk factors in Hispanics. Genotype frequencies were as follows: CC, 52.9%; CT, 40.3%; and TT, 6.8%. There were no significant differences in systolic blood pressure, diastolic blood pressure, age, weight, fasting and post-load glucose levels, LDL and HDL cholesterol, triglyceride and urinary albumin levels in subjects with CC, CT or the TT genotypes. Presence of the T allele was associated with increased salt sensitivity in women, but not in men.NO metabolite excretion was markedly decreased both in women and men with the TT genotype (CC: 868779 lmol/day; CT: 839775 lmol/day; TT: 5347 78 lmol/day; Po0.05). In conclusion, the prevalence of the NAD(P)H oxidase p22phox gene C242T polymorphism in Venezuelans was comparable to that of Caucasians, but different from that of Chinese and Japanese. Although the T allele was not associated with cardiovascular risk factors, hyperinsulinaemia or hypertension, in women, it appeared to be a genetic susceptibility factor for salt sensitivity. Both in women and men, the p22phox gene may play a role in the genetic control of NO levels.

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“…Several enzymes have been implicated as possible sources of elevated ROS in hypertension, including NADPH oxidase, 14,15 xanthine oxidase, 16 NO synthase (NOS), 17 cyclooxygenase, 18 and mitochondrial electron transport leakage. 19 It has been suggested that reductions of enzymes that scavenge ROS, such as superoxide dismutases (SOD), 20 catalase, and glutathione peroxidase (GPx), may also play a role. In the present study, we explored which of these many pathways most importantly determines the susceptibility of the SS rat to salt-induced hypertension.…”

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confidence: 99%

NADPH Oxidase in the Renal Medulla Causes Oxidative Stress and Contributes to Salt-Sensitive Hypertension in Dahl S Rats

et al. 2006

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Abstract-Dahl salt-sensitive (SS) rats exhibit increased renal medullary oxidative stress and blood pressure salt-sensitivity compared with consomic, salt-resistant SS-13 BN rats, despite highly similar genetic backgrounds. The present study examined potential sources of renal medullary superoxide in prehypertensive SS rats fed a 0.4% NaCl diet by assessing activity and protein levels of superoxide producing and scavenging enzymes. Superoxide production was nearly doubled in SS rats compared with SS-13 BN rats as determined by urinary 8-isoprostane excretion and renal medullary oxy-ethidium microdialysate levels. Medullary superoxide production in tissue homogenates was greater in SS rats, and the NADPH oxidase inhibitor diphenylene iodonium preferentially reduced SS levels to those found in SS-13 BN rats. Dinitrophenol, a mitochondrial uncoupler, eliminated the remaining superoxide production in both strains, whereas inhibition of xanthine oxidase, NO synthase, and cycloxygenase had no effect. L-arginine, NO synthase, superoxide dismutase, catalase, and glutathione peroxidase activities between SS and SS-13 BN rats did not differ. Chronic blood pressure responses to a 4% NaCl diet were then determined in the presence or absence of the NADPH oxidase inhibitor apocynin (3.5 g/kg per minute), chronically delivered directly into the renal medulla. Apocynin infusion reduced renal medullary interstitial superoxide from 1059Ϯ130 to 422Ϯ80 (oxyethidium fluorescence units) and mean arterial pressure from 175Ϯ4 to 157Ϯ6 mm Hg in SS rats, whereas no effects on either were observed in the SS-13 BN . We conclude that excess renal medullary superoxide production in SS rats contributes to salt-induced hypertension, and NADPH oxidase is the major source of the excess superoxide.

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Superoxide dismutase and oxidative stress in Dahl salt-sensitive and -resistant rats

Cited by 133 publications

References 31 publications

Salt Intake, Oxidative Stress, and Renal Expression of NADPH Oxidase and Superoxide Dismutase

Salt Intake, Oxidative Stress, and Renal Expression of NADPH Oxidase and Superoxide Dismutase

NAD(P)H oxidase p22phox gene C242T polymorphism, nitric oxide production, salt sensitivity and cardiovascular risk factors in Hispanics

NADPH Oxidase in the Renal Medulla Causes Oxidative Stress and Contributes to Salt-Sensitive Hypertension in Dahl S Rats

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