scholarly journals Ascorbic acid or l-arginine improves cutaneous microvascular function in chronic kidney disease

2011 ◽  
Vol 111 (6) ◽  
pp. 1561-1567 ◽  
Author(s):  
Jennifer J. DuPont ◽  
William B. Farquhar ◽  
Raymond R. Townsend ◽  
David G. Edwards
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Ascorbic Acid ◽  
Kidney Disease ◽  
Local Heating ◽  
Microvascular Function ◽  
Doppler Flowmetry ◽  
Healthy Control ◽  
Cutaneous Vascular Conductance ◽  
Initial Peak

We sought to determine whether oxidative stress or a relative deficit of l-arginine plays a role in reducing cutaneous vasodilation in response to local heating in chronic kidney disease (CKD). Eight patients with stage 3–4 CKD and eight age- and sex-matched healthy control (HC) subjects were instrumented with four microdialysis (MD) fibers for the local delivery of 1) Ringers solution (R), 2) 20 mM ascorbic acid (AA), 3) 10 mM l-arginine (l-Arg), and 4) 10 mM NG-nitro-l-arginine methyl ester (l-NAME). Red blood cell (RBC) flux was measured via laser Doppler flowmetry. A standardized nonpainful local heating protocol (42°C) was used. Cutaneous vascular conductance (CVC) was calculated as RBC flux/MAP and all data were expressed as a percentage of the maximum CVC at each site (28 mM sodium nitroprusside, Tloc = 43°C). The plateau %CVCmax was attenuated in CKD (CKD: 76 ± 4 vs. HC: 91 ± 2%CVCmax; P < 0.05) and the NO contribution to the plateau was lower in CKD (CKD: 39 ± 7, HC: 54 ± 5; P < 0.05). The plateau %CVCmax in the CKD group was significantly greater at the AA and l-Arg sites compared with R (AA: 89 ± 2; l-Arg: 90 ± 1; R: 76 ± 4; P < 0.05) and did not differ from HC. Initial peak %CVCmax was also significantly attenuated at the R and l-Arg sites in CKD ( P < 0.05) but did not differ at the AA site. These results suggest that cutaneous microvascular function is impaired in stage 3–4 CKD and that oxidative stress and a deficit of l-arginine play a role in this impairment.

Abstract 209: NAD(P)H Oxidase-Derived Superoxide Contributes to Impaired Cutaneous Microvascular Function in Chronic Kidney Disease

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Jennifer J DuPont ◽  
Meghan G Ramick ◽  
William B Farquhar ◽  
Raymond R Townsend ◽  
David G Edwards
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Xanthine Oxidase ◽  
Local Heating ◽  
Control Site ◽  
Healthy Control Group ◽  
Control Group ◽  
Doppler Flowmetry ◽  
Cutaneous Vasodilation ◽  
Healthy Control

Endothelial dysfunction occurs in chronic kidney disease (CKD) and cardiovascular disease is the most common cause of death in these patients. Oxidative stress has been shown to be a mechanism of vascular dysfunction in CKD. We utilized the cutaneous circulation to test the hypothesis that superoxide derived from NAD(P)H oxidase and xanthine oxidase impair nitric oxide (NO)-dependent cutaneous vasodilation patients with CKD. Twenty subjects, 10 stage 3 and 4 CKD patients (61±4 years; 5 male/5 female; eGFR: 39 ± 4 ml·min -1 ·1.73m -2 ) and 10 healthy controls (HC) (55±2 years; 4 male/6 female; eGFR: >60 ml·min -1 ·1.73m -2 ) were instrumented with 4 intradermal microdialysis fibers in the forearm for the local delivery of 1) Ringers solution (Control), 2) 10 μM Tempol to scavenge superoxide, 3) 100 μM apocynin to inhibit NAD(P)H oxidase, and 4) 10 μM allopurinol to inhibit xanthine oxidase. Red blood cell (RBC) flux was measured via laser Doppler flowmetry during standardized local heating (42°C). After the local heating response was established, 10 mM L-NAME was infused into all four sites to quantify the NO-dependent portion of the response. Cutaneous vascular conductance (CVC) was calculated as RBC flux/mean arterial pressure and all data are presented as a percentage of maximum CVC achieved during 28mM sodium nitroprusside infusion at 43°C. The plateau in cutaneous vasodilation was attenuated in CKD at the control site (CKD: 77±3 vs. HC: 88±3 %, p<0.05). Tempol and apocynin augmented the plateau in cutaneous vasodilation in CKD patients (Tempol: 88±2, apocynin: 91±2 %, p<0.05 vs. CKD control site) but had no effect in the healthy control group. The NO-dependent portion of the response was reduced in CKD at the control site (CKD: 41±4 vs. HC: 58±2 %, p<0.05). Tempol and apocynin augmented NO-dependent portion of the response in CKD patients (Tempol: 58±3, apocynin: 58±4 %, p<0.05 vs. CKD control site) but had no effect in the healthy control group. Inhibition of xanthine oxidase did not alter the plateau in cutaneous vasodilation in either group (p>0.05). These data suggest that NAD(P)H oxidase is a source of superoxide and contributes to microvascular dysfunction in CKD.

scholarly journals Role of mitochondria-derived reactive oxygen species in microvascular dysfunction in chronic kidney disease

2018 ◽  
Vol 314 (3) ◽  
pp. F423-F429 ◽  
Author(s):  
Danielle L. Kirkman ◽  
Bryce J. Muth ◽  
Meghan G. Ramick ◽  
Raymond R. Townsend ◽  
David G. Edwards
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Local Heating ◽  
Reactive Oxygen ◽  
Microvascular Dysfunction ◽  
Healthy Controls ◽  
Oxygen Species ◽  
Cutaneous Vasodilation

Cardiovascular disease is the leading cause of mortality in chronic kidney disease (CKD). Mitochondrial dysfunction secondary to CKD is a potential source of oxidative stress that may impair vascular function. This study sought to determine if mitochondria-derived reactive oxygen species contribute to microvascular dysfunction in stage 3–5 CKD. Cutaneous vasodilation in response to local heating was assessed in 20 CKD patients [60 ± 13 yr; estimated glomerular filtration rate (eGFR) 46 ± 13 ml·kg−1·1.73 m−2] and 11 matched healthy participants (58 ± 2 yr; eGFR >90 ml·kg−1·1.73 m−2). Participants were instrumented with two microdialysis fibers for the delivery of 1) Ringer solution, and 2) the mitochondria- specific superoxide scavenger MitoTempo. Skin blood flow was measured via laser Doppler flowmetry during standardized local heating (42°C). Cutaneous vascular conductance (CVC) was calculated as a percentage of the maximum conductance achieved with sodium nitroprusside infusion at 43°C. Urinary isofuran/F2-isoprostane ratios were assessed by gas-chromatography mass spectroscopy. Isofuran-to-F2-isoprostane ratios were increased in CKD patients (3.08 ± 0.32 vs. 1.69 ± 0.12 arbitrary units; P < 0.01) indicative of mitochondria-derived oxidative stress. Cutaneous vasodilation was impaired in CKD compared with healthy controls (87 ± 1 vs. 92 ± 1%CVCmax; P < 0.01). Infusion of MitoTempo significantly increased the plateau phase CVC in CKD patients (CKD Ringer vs. CKD MitoTempo: 87 ± 1 vs. 93 ± 1%CVCmax; P < 0.01) to similar levels observed in healthy controls ( P = 0.9). These data provide in vivo evidence that mitochondria-derived reactive oxygen species contribute to microvascular dysfunction in CKD and suggest that mitochondrial dysfunction may be a potential therapeutic target to improve CKD-related vascular dysfunction.

scholarly journals Acute Thermotherapy Prevents Impairments in Cutaneous Microvascular Function Induced by a High Fat Meal

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Jennifer C. Harvey ◽  
Bruno T. Roseguini ◽  
Benjamin M. Goerger ◽  
Elizabeth A. Fallon ◽  
Brett J. Wong
Keyword(s):  
Blood Pressure ◽  
Local Heating ◽  
Microvascular Function ◽  
High Fat ◽  
Vascular Conductance ◽  
Blood Samples ◽  
Cutaneous Vasodilation ◽  
Cutaneous Vascular Conductance ◽  
Initial Peak ◽  
Fat Meal

We tested the hypothesis that a high fat meal (HFM) would impair cutaneous vasodilation, while thermotherapy (TT) would reverse the detrimental effects. Eight participants were instrumented with skin heaters and laser-Doppler (LD) probes and tested in three trials: control, HFM, and HFM + TT. Participants wore a water-perfused suit perfused with 33°C (control and HFM) or 50°C (HFM + TT) water. Participants consumed 1 g fat/kg body weight. Blood samples were taken at baseline and two hours post-HFM. Blood pressure was measured every 5–10 minutes. Microvascular function was assessed via skin local heating from 33°C to 39°C two hours after HFM. Cutaneous vascular conductance (CVC) was calculated and normalized to maximal vasodilation (%CVCmax). HFM had no effect on initial peak (48 ± 4 %CVCmax) compared to control (49 ± 4 %CVCmax) but attenuated the plateau (51 ± 4 %CVCmax) compared to control (63 ± 4 %CVCmax,P< 0.001). Initial peak was augmented in HFM + TT (66 ± 4 %CVCmax) compared to control and HFM (P< 0.05), while plateau (73 ± 3 %CVCmax) was augmented only compared to the HFM trial (P< 0.001). These data suggest that HFM negatively affects cutaneous vasodilation but can be minimized by TT.

scholarly journals Nitric Oxide-mediated Cutaneous Microvascular Function is not Altered in Young Adults Following Mild-to-Moderate SARS CoV-2 Infection.

2022 ◽  
Author(s):  
Gabrielle A. Dillon ◽  
S. Tony Wolf ◽  
Lacy M. Alexander
Keyword(s):  
Nitric Oxide ◽  
Vascular Dysfunction ◽  
Local Heating ◽  
Cross Sectional Study ◽  
Healthy Adults ◽  
Microvascular Function ◽  
Cross Sectional ◽  
Doppler Flowmetry ◽  
Healthy Control ◽  
Underlying Mechanisms

Vascular dysfunction has been reported in adults who have recovered from COVID-19. To date, no studies have investigated the underlying mechanisms of persistent COVID-19-associated vascular dysfunction. PURPOSE: To quantify nitric oxide (NO)-mediated vasodilation in healthy adults who have recovered from SARS-CoV-2 infection. We hypothesized that COVID-19-recovered adults would have impaired NO-mediated vasodilation compared to adults who have not had COVID-19. METHODS: We performed a cross-sectional study including: 10 (5M/5W, 24 ± 4yrs) healthy control (HC) adults who were unvaccinated for COVID-19, 11 (4M/7W, 25 ± 6yrs) healthy vaccinated (HV) adults, and 12 (5M/7W, 22 ± 3yrs) post-COVID-19 (PC, 19 ± 14wks) adults. COVID-19 symptoms severity (survey) were assessed. A standardized 39°C local heating protocol was used to assess NO-dependent vasodilation via perfusion (intradermal microdialysis) of 15 mM NG-nitro-l-arginine methyl ester during the plateau of the heating response. Red blood cell flux was measured (laser-Doppler flowmetry) and cutaneous vascular conductance (CVC = flux/mmHg) was expressed as a percentage of maximum (28mM sodium nitroprusside + 43°C). RESULTS: The local heating plateau (HC: 61 ± 20%, HV: 60 ± 19%, PC: 67 ± 19%, p=0.80) and NO-dependent vasodilation (HC: 77 ± 9%, HV: 71 ± 7%, PC: 70 ± 10%, p=0.36) were not different among groups. Neither symptom severity (25 ± 12 AU) nor time since diagnosis correlated with the NO-dependent vasodilation (r=0.46, p=0.13; r=0.41, p=0.19, respectively). CONCLUSION: Healthy adults who have had mild-to-moderate COVID-19 do not have altered NO-mediated cutaneous microvascular function.

scholarly journals Recurrent Indoor Environmental Pollution and Its Impact on Health and Oxidative Stress of the Textile Workers in Bangladesh

2020 ◽  
Vol 14 ◽  
pp. 117863022093839
Author(s):  
Tania Rahman ◽  
Ar-Rafi Md. Faisal ◽  
Tahura Khanam ◽  
Hossain Uddin Shekhar
Keyword(s):  
Oxidative Stress ◽  
Ascorbic Acid ◽  
Occupational Health ◽  
Environmental Pollution ◽  
Control Area ◽  
Textile Workers ◽  
Control Subjects ◽  
Oxidative Stresses ◽  
Healthy Control ◽  
Textile Industries

Perennial indoor environmental pollution in the textile industrial area is a potential health hazard for workers engaged in this line of work, resulting in mental aberration to severe health risks. This study was designed to investigate the indoor environmental quality of textile industries and correlate its effect on the occupational health and well-being of the textile workers by measuring plasma oxidative stress status in textile workers and healthy control subjects. Environmental samples were collected from 15 textile industries located in Dhaka division, and 30 volunteer textile workers and 30 volunteer office workers (control) aged 18 to 57 years participated in the study. The concentration of plasma ascorbic acid (P-ASC), plasma malondialdehyde (P-MDA), and plasma conjugated diene (P-CD) was measured in both groups. The noise level (78.0 ± 0.68 dB) and the formaldehyde level (141.80 ± 4.47 µg/m3) were found to be significantly higher in the indoor environmental area compared with those in the control area (70.17 ± 0.25 dB and 108.0 ± 0.76 µg/m3, respectively). Furthermore, the daily average concentration of suspended particulate matters (PMs), that is, PM2.5 (322.2 ± 13.46 µg/m3) and PM10 (411.0 ± 17.57 µg/m3), was also found to be significantly higher in the indoor environmental air compared with that in the control area (78.59 ± 1.66 and 174.0 ± 2.33 µg/m3, respectively). The levels of P-MDA (0.37 ± 0.03 nmol/L) and P-CD (14.74 ± 0.61 nmol/L) were significantly increased, whereas the level of P-ASC level (0.46 ± 0.04 mg/dL) was markedly decreased in the textile workers compared with the healthy control subjects (0.18 ± 0.01 nmol/L of P-MDA, 10.04 ± 0.44 nmol/L of P-CD, and 1.29 ± 0.06 mg/dL of P-ASC). The textile plants were found to have significantly elevated levels of indoor environmental pollutants compared with those in the control area, and the textile workers were significantly exposed to oxidative stresses compared with the control subjects. The use of noise pads and high-efficiency air filters is perhaps highly instrumental to put an end to this prevailing situation. Moreover, to overcome the oxidative stresses among workers, supplementation of antioxidant vitamins (ie, ascorbic acid and/or vitamin E) may be beneficial. In addition, to prevent serious health-related issues, proper precautions should be taken to protect the occupational health of the textile workers.

scholarly journals Oxidative Stress in Non-Dialysis-Dependent Chronic Kidney Disease Patients

2021 ◽  
Vol 18 (15) ◽  
pp. 7806
Author(s):  
Patricia Tomás-Simó ◽  
Luis D’Marco ◽  
María Romero-Parra ◽  
Mari Carmen Tormos-Muñoz ◽  
Guillermo Sáez ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Reduced Glutathione ◽  
Genetic Material ◽  
Future Research ◽  
Control Group ◽  
Dialysis Patients ◽  
Early Stages ◽  
Molecular Lines

Background: Cardiovascular complications are the leading cause of morbidity and mortality at any stage of chronic kidney disease (CKD). Moreover, the high rate of cardiovascular mortality observed in these patients is associated with an accelerated atherosclerosis process that likely starts at the early stages of CKD. Thus, traditional and non-traditional or uremic-related factors represent a link between CKD and cardiovascular risk. Among non-conventional risk factors, particular focus has been placed on anaemia, mineral and bone disorders, inflammation, malnutrition and oxidative stress and, in this regard, connections have been reported between oxidative stress and cardiovascular disease in dialysis patients. Methods: We evaluated the oxidation process in different molecular lines (proteins, lipids and genetic material) in 155 non-dialysis patients at different stages of CKD and 45 healthy controls. To assess oxidative stress status, we analyzed oxidized glutathione (GSSG), reduced glutathione (GSH) and the oxidized/reduced glutathione ratio (GSSG/GSH) and other oxidation indicators, including malondialdehyde (MDA) and 8-oxo-2’-deoxyguanosine (8-oxo-dG). Results: An active grade of oxidative stress was found from the early stages of CKD onwards, which affected all of the molecular lines studied. We observed a heightened oxidative state (indicated by a higher level of oxidized molecules together with decreased levels of antioxidant molecules) as kidney function declined. Furthermore, oxidative stress-related alterations were significantly greater in CKD patients than in the control group. Conclusions: CKD patients exhibit significantly higher oxidative stress than healthy individuals, and these alterations intensify as eGFR declines, showing significant differences between CKD stages. Thus, future research is warranted to provide clearer results in this area.

scholarly journals Oxidative stress increases 1-deoxysphingolipid levels in chronic kidney disease

2021 ◽  
Vol 164 ◽  
pp. 139-148
Author(s):  
Ting Gui ◽  
Yunlun Li ◽  
Shijun Zhang ◽  
Irina Alecu ◽  
Qingfa Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Kidney Disease

scholarly journals Indoxyl-Sulfate-Induced Redox Imbalance in Chronic Kidney Disease

Antioxidants ◽  
2021 ◽  
Vol 10 (6) ◽  
pp. 936
Author(s):  
Chien-Lin Lu ◽  
Cai-Mei Zheng ◽  
Kuo-Cheng Lu ◽  
Min-Tser Liao ◽  
Kun-Lin Wu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Muscle Wasting ◽  
Mesangial Cells ◽  
Target Organ Damage ◽  
Organ Damage ◽  
Indoxyl Sulfate ◽  
Uremic Toxin ◽  
Tubulointerstitial Injury

The accumulation of the uremic toxin indoxyl sulfate (IS) induces target organ damage in chronic kidney disease (CKD) patients, and causes complications including cardiovascular diseases, renal osteodystrophy, muscle wasting, and anemia. IS stimulates reactive oxygen species (ROS) production in CKD, which impairs glomerular filtration by a direct cytotoxic effect on the mesangial cells. IS further reduces antioxidant capacity in renal proximal tubular cells and contributes to tubulointerstitial injury. IS-induced ROS formation triggers the switching of vascular smooth muscular cells to the osteoblastic phenotype, which induces cardiovascular risk. Low-turnover bone disease seen in early CKD relies on the inhibitory effects of IS on osteoblast viability and differentiation, and osteoblastic signaling via the parathyroid hormone. Excessive ROS and inflammatory cytokine releases caused by IS directly inhibit myocyte growth in muscle wasting via myokines’ effects. Moreover, IS triggers eryptosis via ROS-mediated oxidative stress, and elevates hepcidin levels in order to prevent iron flux in circulation in renal anemia. Thus, IS-induced oxidative stress underlies the mechanisms in CKD-related complications. This review summarizes the underlying mechanisms of how IS mediates oxidative stress in the pathogenesis of CKD’s complications. Furthermore, we also discuss the potential role of oral AST-120 in attenuating IS-mediated oxidative stress after gastrointestinal adsorption of the IS precursor indole.

scholarly journals Inflammation, Oxidative Stress, and Bone in Chronic Kidney Disease in the Osteoimmunology Era

2021 ◽  
Author(s):  
Sandro Mazzaferro ◽  
◽  
Domenico Bagordo ◽  
Natalia De Martini ◽  
Marzia Pasquali ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Kidney Disease

scholarly journals Association of Sarcopenia and Gut Microbiota Composition in Older Patients with Advanced Chronic Kidney Disease, Investigation of the Interactions with Uremic Toxins, Inflammation and Oxidative Stress

Toxins ◽  
2021 ◽  
Vol 13 (7) ◽  
pp. 472
Author(s):  
Elisabetta Margiotta ◽  
Lara Caldiroli ◽  
Maria Luisa Callegari ◽  
Francesco Miragoli ◽  
Francesca Zanoni ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Gut Microbiota ◽  
Inflammatory Cytokines ◽  
Interleukin 10 ◽  
Uremic Toxins ◽  
Interleukin 12 ◽  
European Working ◽  
And Oxidative Stress

Background: Sarcopenia is a prevalent condition in chronic kidney disease (CKD). We determined gut microbiota (gMB) composition in CKD patients with or without sarcopenia. Furthermore, we investigated whether in these patients, there was any association between gMB, uremic toxins, inflammation and oxidative stress. Methods: We analyzed gMB composition, uremic toxins (indoxyl sulphate and p-cresyl sulphate), inflammatory cytokines (interleukin 10, tumor necrosis factor α, interleukin 6, interleukin 17, interleukin 12 p70, monocyte chemoattractant protein-1 and fetuin-A) and oxidative stress (malondialdehyde) of 64 elderly CKD patients (10 < eGFR < 45 mL/min/1.73 m2, not on dialysis) categorized as sarcopenic and not-sarcopenic. Sarcopenia was defined according to European Working Group on Sarcopenia in Older People 2 criteria. Results: Sarcopenic patients had a greater abundance of the Micrococcaceae and Verrucomicrobiaceae families and of Megasphaera, Rothia, Veillonella, Akkermansia and Coprobacillus genera. They had a lower abundance of the Gemellaceae and Veillonellaceae families and of Acidaminococcus and Gemella genera. GMB was associated with uremic toxins, inflammatory cytokines and MDA. However, uremic toxins, inflammatory cytokines and MDA were not different in sarcopenic compared with not-sarcopenic individuals, except for interleukin 10, which was higher in not-sarcopenic patients. Conclusions: In older CKD patients, gMB was different in sarcopenic than in not-sarcopenic ones. Several bacterial families and genera were associated with uremic toxins and inflammatory cytokines, although none of these latter substantially different in sarcopenic versus not-sarcopenic patients.

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