Impact of elevated dietary sodium intake on NAD(P)H oxidase and SOD in the cortex and medulla of the rat kidney

Johns, Edward J.; O’Shaughnessy, Ben; O'Neill, Susan; Lane, Bill; Healy, Vincent

doi:10.1152/ajpregu.00541.2009

Cited by 24 publications

(15 citation statements)

References 27 publications

(40 reference statements)

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“…These findings are consistent with earlier studies. 32 Superoxide can directly influence tubular reabsorption of sodium 33,34 in setting of hypertension 5 and renal injury in obese rats as seen in the present study and in Dahl S (salt-sensitive) rats. 35 The AT 2 R agonist C21 treatment has shown to reduce renal Ang-II, 5 expression of p47phox – NOX subunit, 36 superoxide formation 37 and salt-sensitive rise in blood pressure.…”

Section: Discussionsupporting

confidence: 60%

Angiotensin II Type 2–Receptor Agonist C21 Reduces Proteinuria and Oxidative Stress in Kidney of High-Salt–Fed Obese Zucker Rats

2016

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Oxidative and nitrosative stress have been implicated in high sodium diet (HSD)-related hypertensive renal injury. In the present study we investigated AT2R-mediated renoprotection in obese Zucker rats fed HSD. Obese Zucker rats were fed normal sodium-diet (NSD) or HSD 4%, for 14 days, with/without AT2R agonist C21, delivered subcutaneously via osmotic pump, 1 mg/kg/day. Compared to NSD controls, HSD rats exhibited increase in cortical NADPH oxidase activity, urinary H2O2 and 8-isoprostanes, which were associated with severe glomerulosclerosis, interstitial fibrosis, decline in estimated glomerular filtration rate (eGFR), and an increase in urinary leak and activity of N-acetyl-β-D-glucosaminidase, a lysosomal enzyme and a marker of tubular damage. These changes were improved by C21 treatment. Cortical expression of endothelial nitric oxide synthase (eNOS), p-eNOS (Ser1177) and plasma nitrites were reduced after HSD intake while nitrosative stress (3-nitrotyrosine) and enzymatic defense (superoxide dismutase-to-catalase activity) remained unaltered. Albeit, C21 preserved plasma nitrites in HSD-fed OZR. C21 treatment reduced protein-to-creatinine (uPcr), albumin-to-creatinine (uAcr) as well as fractional excretion of protein (FEpro) and albumin (FEalb) in HSD-fed OZR, which is independent of changes in protein recycling receptors, megalin and cubilin. HSD intake also altered renal excretory and reabsorptive capacity as evident by elevated plasma urea nitrogen-to-creatinine (UN-to-cr) and fractional excretion of urea nitrogen (FEUN), and reduced urine-to-plasma creatinine (UPcr), which were modestly, but insignificantly, improved by C21 treatment. Together results demonstrate that AT2R activation protects against HSD-induced kidney damage in obesity plausibly by reducing NOX activity and rescuing nitrites.

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Section: Discussionsupporting

confidence: 60%

Angiotensin II Type 2–Receptor Agonist C21 Reduces Proteinuria and Oxidative Stress in Kidney of High-Salt–Fed Obese Zucker Rats

2016

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“…This latter observation was unexpected but was probably the result of the anesthesia and stress involved in the surgical preparation as we have reported previously (17) that in the conscious state sodium excretion is markedly elevated in rats fed a high-sodium diet.…”

Section: R264 Dietary Sodium Intake and Ang (1-7)-induced Diuresis Anmentioning

confidence: 48%

Dietary sodium intake modulates renal excretory responses to intrarenal angiotensin (1–7) administration in anesthetized rats

O’Neill

Corbett

Johns

2013

American Journal of Physiology-Regulatory, Integrative and Comp

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O'Neill J, Corbett A, Johns EJ. Dietary sodium intake modulates renal excretory responses to intrarenal angiotensin (1-7) administration in anesthetized rats. Am J Physiol Regul Integr Comp Physiol 304: R260 -R266, 2013. First published December 19, 2012 doi:10.1152/ajpregu.00583.2011-Angiotensin II at the kidney regulates renal hemodynamic and excretory function, but the actions of an alternative metabolite, angiotensin (1-7), are less clear. This study investigated how manipulation of dietary sodium intake influenced the renal hemodynamic and excretory responses to intrarenal administration of angiotensin (1-7). Renal interstitial infusion of angiotensin (1-7) in anesthetized rats fed a normal salt intake had minimal effects on glomerular filtration rate but caused dose-related increases in urine flow and absolute and fractional sodium excretions ranging from 150 to 200%. In rats maintained for 2 wk on a low-sodium diet angiotensin (1-7) increased glomerular filtration rate by some 45%, but the diuretic and natriuretic responses were enhanced compared with those in rats on a normal sodium intake. By contrast, renal interstitial infusion of angiotensin (1-7) in rats maintained on a high-sodium intake had no effect on glomerular filtration rate, whereas the diuresis and natriuresis was markedly attenuated compared with those in rats fed either a normal or low-sodium diet. Plasma renin and angiotensin (1-7) were highest in the rats on the low-sodium diet and depressed in the rats on a high-sodium diet. These findings demonstrate that the renal hemodynamic and excretory responses to locally administered angiotensin (1-7) is dependent on the level of sodium intake and indirectly on the degree of activation of the renin-angiotensin system. The exact way in which angiotensin (1-7) exerts its effects may be dependent on the prevailing levels of angiotensin II and its receptor expression.angiotensin (1-7); dietary sodium; renal hemodynamics; sodium excretion THE RENIN ANGIOTENSIN SYSTEM (RAS) is a powerful endogenous hormonal cascade that plays a central role in the regulation of blood pressure, sodium balance, and body fluid homeostasis. Classically, this cascade culminates in the formation of the potent vasoconstrictor, antinatriuretic and antidiuretic peptide angiotensin II (ANG II) (7,20). ANG II is produced from angiotensin I (ANG I) primarily via angiotensin-converting enzyme (ACE) but also via the tissue enzyme chymase. The latter has been shown to contribute to the production of ANG II in the diabetic mouse kidney (21). More recently, another RAS peptide called angiotensin (1-7) [ANG (1-7)] has been described as the endogenous counter regulator of ANG II (16) via activation of its "mas" receptor (24). ANG (1-7) is formed directly from ANG II by the ACE isoform ACE 2 (27, 32) but can also be synthesized directly from ANG I via tissue-specific peptidases such as neprilysin in the kidney (2).The intrarenal actions of ANG (1-7) and its interaction with ANG II on renal hemodynamics and tubular fluid reabsorption h...

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“…Three additional groups of CIH-treated rats (5% O 2 at the nadir; 2 weeks) had free access to water containing N-acetyl cysteine (1% NAC, n = 8), tempol (1 mM, n = 8) or apocynin (2 mM, n = 8), beginning 1 day prior to treatment and continuing throughout the 2 week study. Doses were informed by previous published studies (Dunleavy et al 2008;Johns et al 2010;Skelly et al 2012).…”

Section: Chronic Antioxidant/apocynin Supplementation In Cih-treated mentioning

confidence: 99%

Reactive oxygen species mediated diaphragm fatigue in a rat model of chronic intermittent hypoxia

Shortt

Fredsted

Chow

et al. 2014

Experimental Physiology

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New Findings r What is the central question of this study?The effects of chronic intermittent hypoxia (CIH) on respiratory muscles are relatively underexplored. It is speculated that muscle dysfunction and other key morbidities associated with sleep apnoea are the result of CIH-induced oxidative stress. We sought to investigate the putative role of CIH-induced reactive oxygen species in the development of respiratory muscle dysfunction. r What is the main finding and its importance?The CIH-induced diaphragm muscle fatigue is time and intensity dependent and is associated with a modest oxidative stress. Supplementation with N-acetyl cysteine prevents CIH-induced diaphragm muscle dysfunction, suggesting that antioxidant supplementation may have therapeutic value in respiratory muscle disorders characterized by CIH, such as obstructive sleep apnoea.Respiratory muscle dysfunction documented in sleep apnoea patients is perhaps due to oxidative stress secondary to chronic intermittent hypoxia (CIH). We sought to explore the effects of different CIH protocols on respiratory muscle form and function in a rodent model. Adult male Wistar rats were exposed to CIH (n = 32) consisting of 90 s normoxia-90 s hypoxia (either 10 or 5% oxygen at the nadir; arterial O 2 saturation ß90 or 80%, respectively] for 8 h per day or to sham treatment (air-air, n = 32) for 1 or 2 weeks. Three additional groups of CIH-treated rats (5% O 2 for 2 weeks) had free access to water containing N-acetyl cysteine (1% NAC, n = 8), tempol (1 mm, n = 8) or apocynin (2 mm, n = 8). Functional properties of the diaphragm muscle were examined ex vivo at 35°C. The myosin heavy chain and sarco(endo)plasmic reticulum Ca 2+ -ATPase isoform distribution, succinate dehydrogenase and glyercol phosphate dehydrogenase enzyme activities, Na + -K + -ATPase pump content, concentration of thiobarbituric acid reactive substances, DNA oxidation and antioxidant capacity were determined. Chronic intermittent hypoxia (5% oxygen at the nadir; 2 weeks) decreased diaphragm muscle force and endurance. All three drugs reversed the deleterious effects of CIH on diaphragm endurance, but only NAC prevented CIH-induced diaphragm weakness. Chronic intermittent hypoxia increased diaphragm muscle myosin heavy chain 2B areal density and oxidized glutathione/reduced glutathione (GSSG/GSH) ratio. We conclude that CIH-induced diaphragm dysfunction is reactive oxygen species dependent. N-Acetyl cysteine was most effective in reversing CIH-induced effects on diaphragm. Our results suggest that respiratory muscle dysfunction in sleep apnoea may be the result of oxidative stress and, as such, antioxidant treatment could prove a useful adjunctive therapy for the disorder. DOI

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Impact of elevated dietary sodium intake on NAD(P)H oxidase and SOD in the cortex and medulla of the rat kidney

Cited by 24 publications

References 27 publications

Angiotensin II Type 2–Receptor Agonist C21 Reduces Proteinuria and Oxidative Stress in Kidney of High-Salt–Fed Obese Zucker Rats

Angiotensin II Type 2–Receptor Agonist C21 Reduces Proteinuria and Oxidative Stress in Kidney of High-Salt–Fed Obese Zucker Rats

Dietary sodium intake modulates renal excretory responses to intrarenal angiotensin (1–7) administration in anesthetized rats

Reactive oxygen species mediated diaphragm fatigue in a rat model of chronic intermittent hypoxia

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