High salt diet impairs memory-related synaptic plasticity via increased oxidative stress and suppressed synaptic protein expression

D 3 dopamine receptor (D 3 R) deficient mice have renin-dependent hypertension but the hypertension is mild and is not associated with oxidative stress. In order to determine if any compensatory mechanism in the kidney is involved in the regulation of blood pressure with disruption of D 3 R, we measured the renal protein expression of dopamine receptors in D 3 R homozygous (D 3 -/-) and heterozygous (D 3 +/-) knockout mice and their wild type (D 3 +/+) littermates. D 5 dopamine receptor (D 5 R) (169±23%, reported as % of D 3 +/+, n=5/group) expression was increased but D 4 dopamine receptors protein expression (59±8%) was decreased, while no significant changes were found with D 1 and D 2 dopamine receptors. Immunocytochemistry showed a stronger renal staining of D 5 R but without a change in renal tubule cell distribution in D 3 -/- relative to D 3 +/+ mice. D 5 R abundance was also increased in D 3 +/- (205±30%, n=5/group) relative to D 3 +/+ mice, while D 1 R abundance was similar between D 3 +/- and D 3 +/+ mice. The increase in D 5 R expression was abolished while blood pressure was increased further in D 3 -/- mice fed a high salt diet. Treatment of the D 1 -like (including D 1 and D 5 receptors) antagonist, SCH23390 , increased the blood pressure to a greater extent in anesthetized D 3 -/- mice than in D 3 +/+ mice (n=4/group), suggesting that the upregulation of D 5 R may modulate the hypertension in mice caused by the disruption of D 3 R. Since dopamine inhibits the NADPH oxidase-induced production of reactive oxygen species (ROS) via the D 5 R, we also measured the protein expression of NOXs in the kidney and isoprostane in the urine. No NADPH oxidase subunit was increased in D 3 -/- and D 3 +/- mice relative to D 3 +/+ mice fed a normal or salt high salt diet, and urinary isoprostane excretion was also similar in D 3 -/- and D 3 +/+ mice. Our findings suggest that the upregulation of D 5 R may minimize the hypertension and prevent oxidative stress in D 3 -/- mice.

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Maternal high‐salt diet during pregnancy impairs synaptic plasticity and memory in offspring

The FASEB Journal ◽

10.1096/fj.202001890r ◽

2021 ◽

Vol 35 (4) ◽

Author(s):

Qian Ge ◽

Xiaoxuan Hu ◽

Ning Ma ◽

Meiqi Sun ◽

Liyun Zhang ◽

...

Keyword(s):

Synaptic Plasticity ◽

High Salt ◽

High Salt Diet ◽

Salt Diet

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High-salt diet enhances hippocampal oxidative stress and cognitive impairment in mice

Neurobiology of Learning and Memory ◽

10.1016/j.nlm.2014.04.010 ◽

2014 ◽

Vol 114 ◽

pp. 10-15 ◽

Cited By ~ 24

Author(s):

Yun-Zi Liu ◽

Ji-Kuai Chen ◽

Zhang-Peng Li ◽

Ting Zhao ◽

Min Ni ◽

...

Keyword(s):

Oxidative Stress ◽

Cognitive Impairment ◽

High Salt ◽

High Salt Diet ◽

Salt Diet

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Cyperus esculentus L. (tigernut) mitigates high salt diet‐associated testicular toxicity in Wistar rats by targeting testicular steroidogenesis, oxidative stress and inflammation

Andrologia ◽

10.1111/and.13780 ◽

2020 ◽

Vol 52 (11) ◽

Author(s):

Justina Nwandimma Nwangwa ◽

Augustine Lishilinimye Udefa ◽

Ernest Atelhe Amama ◽

Inah Onete Inah ◽

Hamza Joseph Ibrahim ◽

...

Keyword(s):

Oxidative Stress ◽

Wistar Rats ◽

High Salt ◽

Testicular Toxicity ◽

Cyperus Esculentus ◽

High Salt Diet ◽

Salt Diet ◽

Testicular Steroidogenesis

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Helicobacter pylori AdaptationIn Vivoin Response to a High-Salt Diet

Infection and Immunity ◽

10.1128/iai.00918-15 ◽

2015 ◽

Vol 83 (12) ◽

pp. 4871-4883 ◽

Cited By ~ 11

Author(s):

John T. Loh ◽

Jennifer A. Gaddy ◽

Holly M. Scott Algood ◽

Silvana Gaudieri ◽

Simon Mallal ◽

...

Keyword(s):

Oxidative Stress ◽

Helicobacter Pylori ◽

High Salt ◽

Mongolian Gerbils ◽

High Salt Diet ◽

Salt Diet ◽

Content Type ◽

Regular Diet ◽

H Pylori ◽

And Oxidative Stress

Helicobacter pyloriexhibits a high level of intraspecies genetic diversity. In this study, we investigated whether the diversification ofH. pyloriis influenced by the composition of the diet. Specifically, we investigated the effect of a high-salt diet (a known risk factor for gastric adenocarcinoma) onH. pyloridiversification within a host. We analyzedH. pyloristrains isolated from Mongolian gerbils fed either a high-salt diet or a regular diet for 4 months by proteomic and whole-genome sequencing methods. Compared to the input strain and output strains from animals fed a regular diet, the output strains from animals fed a high-salt diet produced higher levels of proteins involved in iron acquisition and oxidative-stress resistance. Several of these changes were attributable to a nonsynonymous mutation infur(fur-R88H). Further experiments indicated that this mutation conferred increased resistance to high-salt conditions and oxidative stress. We propose a model in which a high-salt diet leads to high levels of gastric inflammation and associated oxidative stress inH. pylori-infected animals and that these conditions, along with the high intraluminal concentrations of sodium chloride, lead to selection ofH. pyloristrains that are most fit for growth in this environment.

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High-salt diet increases glomerular ACE/ACE2 ratio leading to oxidative stress and kidney damage

Nephrology Dialysis Transplantation ◽

10.1093/ndt/gfr600 ◽

2011 ◽

Vol 27 (5) ◽

pp. 1793-1800 ◽

Cited By ~ 33

Author(s):

Stella Bernardi ◽

Barbara Toffoli ◽

Cristina Zennaro ◽

Christos Tikellis ◽

Silvia Monticone ◽

...

Keyword(s):

Oxidative Stress ◽

Kidney Damage ◽

High Salt ◽

High Salt Diet ◽

Salt Diet

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Melatonin prevents kidney injury in a high salt diet-induced hypertension model by decreasing oxidative stress

Journal of Pineal Research ◽

10.1111/jpi.12287 ◽

2015 ◽

Vol 60 (1) ◽

pp. 48-54 ◽

Cited By ~ 28

Author(s):

Avshalom Leibowitz ◽

Alexander Volkov ◽

Konstantin Voloshin ◽

Chen Shemesh ◽

Iris Barshack ◽

...

Keyword(s):

Oxidative Stress ◽

Kidney Injury ◽

High Salt ◽

High Salt Diet ◽

Salt Diet ◽

Induced Hypertension

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Renoprotection by statins is linked to a decrease in renal oxidative stress, TGF-β, and fibronectin with concomitant increase in nitric oxide bioavailability

AJP Renal Physiology ◽

10.1152/ajprenal.00041.2008 ◽

2008 ◽

Vol 295 (1) ◽

pp. F53-F59 ◽

Cited By ~ 65

Author(s):

Ming-Sheng Zhou ◽

Ivonne Hernandez Schuman ◽

Edgar A. Jaimes ◽

Leopoldo Raij

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

Nadph Oxidase ◽

Protein Expression ◽

Renal Injury ◽

Oxidized Ldl ◽

High Salt ◽

Salt Diet ◽

Enos Activity ◽

Tgf Β1

Clinical and experimental studies have provided evidence suggesting that statins exert renoprotective effects. To investigate the mechanisms by which statins may exert renoprotection, we utilized the hypertensive Dahl salt-sensitive (DS) rat model, which manifests cardiovascular and renal injury linked to increased angiotensin II-dependent activation of NADPH oxidase and decreased nitric oxide (NO) bioavailability. DS rats given high salt diet (4% NaCl) for 10 wk exhibited hypertension [systolic blood pressure (SBP) 200 ± 8 vs. 150 ± 2 mmHg in normal salt diet (0.5% NaCl), P < 0.05], glomerulosclerosis, and proteinuria (158%). This was associated with increased renal oxidative stress demonstrated by urinary 8-F2α-isoprostane excretion and NADPH oxidase activity, increased protein expression of transforming growth factor (TGF)-β (63%) and fibronectin (181%), increased mRNA expression of the proinflammatory molecules monocyte chemoattractant protein-1 (MCP-1) and lectin-like oxidized LDL receptor-1 (LOX-1), as well as downregulation of endothelial NO synthase (eNOS) activity (−44%) and protein expression. Return to normal salt had no effect on SBP or any of the measured parameters. Atorvastatin (30 mg·kg−1·day−1) significantly attenuated proteinuria and glomerulosclerosis and normalized renal oxidative stress, TGF-β1, fibronectin, MCP-1 and LOX-1 expression, and eNOS activity and expression. Atorvastatin-treated rats showed a modest reduction in SBP that remained in the hypertensive range (174 ± 8 mmHg). Atorvastatin combined with removal of high salt normalized SBP and proteinuria. These findings suggest that statins mitigate hypertensive renal injury by restoring the balance among NO, TGF-β1, and oxidative stress and explain the added renoprotective effects observed in clinical studies using statins in addition to inhibitors of the renin-angiotensin system.

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Effect of high-salt diet on mean arterial pressure, renal epithelial sodium channels and aquaporin subunits expression levels in Spontaneously Hypertensive Rats

10.1101/630491 ◽

2019 ◽

Author(s):

Chitra Devi Ramachandran ◽

Khadijeh Gholami ◽

Sau-Kuen Lam ◽

Mohd Rais Mustafa ◽

See-Ziau Hoe

Keyword(s):

Protein Expression ◽

Fluid Intake ◽

High Salt ◽

High Salt Diet ◽

Salt Diet ◽

Spontaneously Hypertensive ◽

Expression Levels ◽

Protein Levels ◽

Wky Rats ◽

Mrna And Protein Expression

AbstractAn increase in blood pressure (BP) by a high-salt (HS) diet may involve the changes in the expression of epithelium sodium channels (ENaCs) and aquaporins (AQPs) in the kidney which affect the sodium- and water-handling mechanisms. In the present study, spontaneously hypertensive rats (SHRs) and Wistar Kyoto (WKY) rats were exposed to HS and regular-salt (RS) diets for 6 weeks and fluid intake was monitored. After 6 weeks, mean arterial pressure (MAP) and plasma hormonal activity of atrial natriuretic peptide (ANP), levels of angiotensin II (Ang II), aldosterone and arginine vasopressin (AVP) were determined. The expression of mRNA and protein levels of ENaC and AQP subunits in kidneys were quantified by real-time PCR and Western blotting. High-salt diet caused higher MAP only in SHRs and higher fluid intake in both strains of rats when compared with their respective controls on RS diet. The plasma levels of Ang II and aldosterone were low in both SHRs and WKY rats fed with HS diet. Meanwhile, plasma ANP activity was high in both strains of rats on HS diet; whilst the AVP showed vice versa effects. The renal expression of mRNA and protein levels of α- and γ-ENaCs was lowered by HS diet in both SHRs and WKY rats. Although β-ENaC mRNA and protein expression levels were depressed in SHRs but they were enhanced in WKY rats. On the other hand, AQP-1, 2 and 7 mRNA and protein expression levels were lowered in both strains of rats fed with HS diet, while that of AQP-3, 4 and 6 showed no significant changes. The suppression of mRNA and protein expression levels of ENaC and AQP subunits suggests that the HS-induced increase in the MAP of SHRs may not be due to the renal sodium and water retention solely.

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Alamandine alleviates hypertension and renal damage via oxidative-stress attenuation in Dahl rats

Cell Death Discovery ◽

10.1038/s41420-022-00822-y ◽

2022 ◽

Vol 8 (1) ◽

Author(s):

Juexiao Gong ◽

Man Luo ◽

Yonghong Yong ◽

Shan Zhong ◽

Peng Li

Keyword(s):

Oxidative Stress ◽

Renal Dysfunction ◽

Renal Damage ◽

High Salt ◽

High Salt Diet ◽

Salt Diet ◽

Renal Tubular Cells ◽

Induced Hypertension

AbstractAlamandine (Ala) is a novel member of the renin–angiotensin-system (RAS) family. The present study aimed to explore the effects of Ala on hypertension and renal damage of Dahl salt-sensitive (SS) rats high-salt diet-induced, and the mechanisms of Ala on renal-damage alleviation. Dahl rats were fed with high-salt diets to induce hypertension and renal damage in vivo, and HK-2 cells were treated with sodium chloride (NaCl) to induce renal injury in vitro. Ala administration alleviated the high-salt diet-induced hypertension, renal dysfunction, and renal fibrosis and apoptosis in Dahl SS rats. The HK-2 cells’ damage, and the increases in the levels of cleaved (c)-caspase3, c-caspase8, and c-poly(ADP-ribose) polymerase (PARP) induced by NaCl were inhibited by Ala. Ala attenuated the NaCl-induced oxidative stress in the kidney and HK-2 cells. DETC, an inhibitor of SOD, reversed the inhibitory effect of Ala on the apoptosis of HK-2 cells induced by NaCl. The NaCl-induced increase in the PKC level was suppressed by Ala in HK-2 cells. Notably, PKC overexpression reversed the moderating effects of Ala on the NaCl-induced apoptosis of HK-2 cells. These results show that Ala alleviates high-salt diet-induced hypertension and renal dysfunction. Ala attenuates the renal damage via inhibiting the PKC/reactive oxygen species (ROS) signaling pathway, thereby suppressing the apoptosis in renal tubular cells.

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