scholarly journals ET-1 increases reactive oxygen species in hypoxic glomeruli during high salt intake

2015 ◽  
Vol 213 (3) ◽  
pp. 559-560 ◽  
Author(s):  
F. Palm
Keyword(s):  
Reactive Oxygen Species ◽  
Salt Intake ◽  
Reactive Oxygen ◽  
High Salt ◽  
Oxygen Species ◽  
High Salt Intake

Reactive oxygen species may contribute to reduced endothelium-dependent dilation in rats fed high salt

2000 ◽  
Vol 279 (1) ◽  
pp. H7-H14 ◽  
Author(s):  
Deborah M. Lenda ◽  
Bryan A. Sauls ◽  
Matthew A. Boegehold
Keyword(s):  
Reactive Oxygen Species ◽  
Salt Intake ◽  
Reactive Oxygen ◽  
High Salt ◽  
Oxygen Species ◽  
Dietary Salt ◽  
No Donor ◽  
High Salt Diet ◽  
Salt Diet ◽  
High Salt Intake

In normotensive rats, an increase in dietary salt leads to decreased arteriolar responsiveness to acetylcholine (ACh) because of suppressed local nitric oxide (NO) activity. We evaluated the possibility that generation of reactive oxygen species in the arteriolar wall is responsible for this loss of NO activity. Arteriolar responses to iontophoretically applied ACh were examined in the superfused spinotrapezius muscle of Sprague-Dawley rats fed a low-salt (LS; 0.45%) or high-salt diet (HS; 7%) for 4–5 wk. Responses to ACh were significantly depressed in HS rats but returned to normal in the presence of the oxidant scavengers superoxide dismutase + catalase or 2,2,6,6-tetamethylpiperidine- N-oxyl (TEMPO) + catalase. Arteriolar responses to the NO donor sodium nitroprusside were similar in HS and LS rats. Arteriolar and venular wall oxidant activity, as determined by reduction of tetranitroblue tetrazolium, was significantly greater in HS rats than in LS rats. Exposure to TEMPO + catalase reduced microvascular oxidant levels to normal in HS rats. These data suggest that a high-salt diet leads to increased generation of reactive oxygen species in striated muscle microvessels, and this increased oxidative state may be responsible for decreased endothelium-dependent responses associated with high salt intake.

Liver Fibrosis Can Be Induced by High Salt Intake through Excess Reactive Oxygen Species (ROS) Production

2016 ◽  
Vol 64 (7) ◽  
pp. 1610-1617 ◽  
Author(s):  
Guang Wang ◽  
Cheung-kwan Yeung ◽  
Wing-Yan Wong ◽  
Nuan Zhang ◽  
Yi-fan Wei ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Liver Fibrosis ◽  
Salt Intake ◽  
Reactive Oxygen ◽  
High Salt ◽  
Ros Production ◽  
Oxygen Species ◽  
High Salt Intake ◽  
Excess Reactive Oxygen Species

scholarly journals Apocynin and Tempol ameliorate dietary sodium-induced declines in cutaneous microvascular function in salt-resistant humans

2019 ◽  
Vol 317 (1) ◽  
pp. H97-H103 ◽  
Author(s):  
Meghan G. Ramick ◽  
Michael S. Brian ◽  
Evan L. Matthews ◽  
Jordan C. Patik ◽  
Douglas R. Seals ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Vascular Function ◽  
Reactive Oxygen ◽  
Microvascular Function ◽  
High Salt ◽  
Dietary Sodium ◽  
Oxygen Species ◽  
High Sodium ◽  
Cutaneous Vasodilation

It has previously been shown that high dietary salt impairs vascular function independent of changes in blood pressure. Rodent studies suggest that NADPH-derived reactive oxygen species mediate the deleterious effect of high salt on the vasculature, and here we translate these findings to humans. Twenty-nine healthy adults (34 ± 2 yr) participated in a controlled feeding study. Participants completed 7 days of a low-sodium diet (LS; 20 mmol sodium/day) and 7 days of a high-sodium diet (HS; 300 mmol sodium/day) in random order. All participants were salt resistant, defined as a ≤5-mmHg change in 24-h mean BP determined while on the LS and HS diets. Laser Doppler flowmetry was used to assess cutaneous vasodilation in response to local heating (42°C) during local delivery of Ringer’s ( n = 29), 20 mM ascorbic acid (AA; n = 29), 10 µM Tempol ( n = 22), and 100 µM apocynin ( n = 22). Additionally, endothelial cells were obtained in a subset of participants from an antecubital vein and stained for nitrotyrosine ( n = 14). Cutaneous vasodilation was attenuated by the HS diet compared with LS [LS 93.0 ± 2.2 vs. HS 86.8 ± 2.0 percentage of maximal cutaneous vascular conductance (%CVCmax); P < 0.05] and was restored by AA during the HS diet (AA 90.7 ± 1.2 %CVCmax; P < 0.05 vs. HS). Cutaneous vasodilation was also restored with the local infusion of both apocynin ( P < 0.01) and Tempol ( P < 0.05) on the HS diet. Nitrotyrosine expression was increased on the HS diet compared with LS ( P < 0.05). These findings provide direct evidence of dietary sodium-induced endothelial cell oxidative stress and suggest that NADPH-derived reactive oxygen species contribute to sodium-induced declines in microvascular function. NEW & NOTEWORTHY High-sodium diets have deleterious effects on vascular function, likely mediating, in part, the increased cardiovascular risk associated with a high sodium intake. Local infusion of apocynin and Tempol improved microvascular function in salt-resistant adults on a high-salt diet, providing evidence that reactive oxygen species contribute to impairments in microvascular function from high salt. This study provides insight into the blood pressure-independent mechanisms by which dietary sodium impairs vascular function. Listen to this article’s corresponding podcast at https://ajpheart.podbean.com/e/dietary-sodium-oxidative-stress-and-microvascular-function/ .

scholarly journals High Salt Enhances Reactive Oxygen Species and Angiotensin II Contractions of Glomerular Afferent Arterioles From Mice With Reduced Renal Mass

Hypertension ◽  
2018 ◽  
Vol 72 (5) ◽  
pp. 1208-1216 ◽  
Author(s):  
Lingli Li ◽  
En Yin Lai ◽  
Zaiming Luo ◽  
Glenn Solis ◽  
Margarida Mendonca ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Angiotensin Ii ◽  
Renal Mass ◽  
Reactive Oxygen ◽  
High Salt ◽  
Oxygen Species ◽  
Afferent Arterioles

scholarly journals Mitochondrial tRNA mutation with high-salt stimulation on cardiac damage: underlying mechanism associated with change of Bax and VDAC

2016 ◽  
Vol 311 (5) ◽  
pp. H1248-H1257 ◽  
Author(s):  
Zhu Chao ◽  
Tian Liuyang ◽  
Li Nan ◽  
Chen Qi ◽  
Cai Zhongqi ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Interventricular Septum ◽  
Reactive Oxygen ◽  
Left Ventricular ◽  
High Salt ◽  
Oxygen Species ◽  
Voltage Dependent Anion Channel ◽  
Mitochondrial Trna ◽  
Cardiac Damage ◽  
Mitochondrial Transfer

Mitochondrial transfer RNA (tRNA) mutation with high-salt stimulation can cause high blood pressure. However, the underlying mechanisms remain unclear. In the present study, we examined the potential molecular mechanisms of cardiac damage caused by mitochondrial tRNA mutation with high-salt stimulation in spontaneously hypertensive rats (SHR). Unanesthetized, 44-wk-old, male, SHR were divided into four groups: SHR, SHR with high-salt stimulation for 8 wk (SHR + NaCl), SHR carrying tRNA mutations (SHR + M), and SHR + M with high-salt stimulation for 8 wk (SHR + M + NaCl). Healthy Wistar-Kyoto (WKY) rats were used as controls. Left ventricular mass and interventricular septum were highest in the SHR + M + NaCl group ( P < 0.05), while ejection fraction was lowest in the SHR + M + NaCl group ( P < 0.05). Hematoxylin and eosin staining showed myocardial cell hypertrophy with interstitial fibrosis and localized inflammatory cell infiltration, in the hypertensive groups, particularly in the SHR + M + NaCl group. Electron microscopy showed different degrees of mitochondrial cavitation in heart tissue of the hypertensive groups, which was highest in the SHR + M + NaCl group. In hypertensive animals, levels of reactive oxygen species were highest in the SHR + M + NaCl group ( P < 0.05). Expression of the voltage-dependent anion channel (VDAC) and the apoptosis regulator Bax were highest in the SHR + M + NaCl group ( P < 0.05), which also showed evidence of VDAC and Bax colocalization ( P < 0.05). Overall, these data suggest that mitochondrial tRNA mutation with high-salt stimulation can aggravate cardiac damage, potentially because of increased expression and interaction between Bax and VDAC and increased reactive oxygen species formation and initiation of apoptosis.

scholarly journals High salt intake shifts the mechanisms of flow-induced dilation in the middle cerebral arteries of Sprague-Dawley rats

2018 ◽  
Vol 315 (3) ◽  
pp. H718-H730 ◽  
Author(s):  
Anita Matic ◽  
Ivana Jukic ◽  
Ana Stupin ◽  
Lidija Baric ◽  
Zrinka Mihaljevic ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Cerebral Arteries ◽  
Hypoxia Inducible Factor ◽  
Reactive Oxygen ◽  
High Salt ◽  
Oxygen Species ◽  
Hypoxia Inducible Factor 1Α ◽  
Middle Cerebral Arteries

The goal of the present study was to examine the effect of 1 wk of high salt (HS) intake and the role of oxidative stress in changing the mechanisms of flow-induced dilation (FID) in isolated pressurized middle cerebral arteries of male Sprague-Dawley rats ( n = 15–16 rats/group). Reduced FID in the HS group was restored by intake of the superoxide scavenger tempol (HS + tempol in vivo group). The nitric oxide (NO) synthase inhibitor Nω-nitro-l-arginine methyl ester, cyclooxygenase inhibitor indomethacin, and selective inhibitor of microsomal cytochrome P-450 epoxidase activity N-(methylsulfonyl)-2-(2-propynyloxy)-benzenehexanamide significantly reduced FID in the low salt diet-fed group, whereas FID in the HS group was mediated by NO only. Cyclooxygenase-2 mRNA (but not protein) expression was decreased in the HS and HS + tempol in vivo groups. Hypoxia-inducible factor-1α and VEGF protein levels were increased in the HS group but decreased in the HS + tempol in vivo group. Assessment by direct fluorescence of middle cerebral arteries under flow revealed significantly reduced vascular NO levels and increased superoxide/reactive oxygen species levels in the HS group. These results suggest that HS intake impairs FID and changes FID mechanisms to entirely NO dependent, in contrast to the low-salt diet-fed group, where FID is NO, prostanoid, and epoxyeicosatrienoic acid dependent. These changes were accompanied by increased lipid peroxidation products in the plasma of HS diet-fed rats, increased vascular superoxide/reactive oxygen species levels, and decreased NO levels, together with increased expression of hypoxia-inducible factor-1α and VEGF. NEW & NOTEWORTHY High-salt (HS) diet changes the mechanisms of flow-induced dilation in rat middle cerebral arteries from a combination of nitric oxide-, prostanoid-, and epoxyeicosatrienoic acid-dependent mechanisms to, albeit reduced, a solely nitric oxide-dependent dilation. In vivo reactive oxygen species scavenging restores flow-induced dilation in HS diet-fed rats and ameliorates HS-induced increases in the transcription factor hypoxia-inducible factor-1α and expression of its downstream target genes.

scholarly journals ET-1 increases reactive oxygen species following hypoxia and high-salt diet in the mouse glomerulus

2014 ◽  
Vol 213 (3) ◽  
pp. 722-730 ◽  
Author(s):  
J. B. Heimlich ◽  
J. S. Speed ◽  
C. J. Bloom ◽  
P. M. O'Connor ◽  
J. S. Pollock ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Reactive Oxygen ◽  
High Salt ◽  
Oxygen Species ◽  
High Salt Diet ◽  
Salt Diet
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