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| 2. |
- Bakker, Emily, et al.
(författare)
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Acute dietary nitrate supplementation improves arterial endothelial function at high altitude : A double-blinded randomized controlled cross over study
- 2015
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Ingår i: Nitric oxide. - : Elsevier BV. - 1089-8603 .- 1089-8611. ; 50, s. 58-64
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Tidskriftsartikel (refereegranskat)abstract
- Introduction: Dietary nitrate (NO3-) supplementation serves as an exogenous source of nitrite (NO3-) and nitric oxide (NO) through the NO3- NO3- NO pathway, and may improve vascular functions during normoxia. The effects of NO3- supplementation in healthy lowlanders during hypobaric hypoxia are unknown. Purpose: Determine the effect of acute oral NO3- supplementation via beetroot juice (BJ) on endothelial function (flow mediated dilation; FMD) in lowlanders at 3700 m. Methods: FMD was measured using ultrasound and Doppler in the brachial artery of 11 healthy subjects (4 females, age 25 +/- 5 yrs; height 1.8 +/- 0.1 m, weight 72 +/- 10 kg) sojourning to high altitude. In a randomized, double-blinded crossover study design, FMD was measured 3 h after drinking BJ (5.0 mmol NO3-) and placebo (PL; 0.003 mmol No-3(-)) supplementation at 3700 m, with a 24-h wash out period between tests. FMD was also measured without any BJ supplementation pre-trek at 1370 m, after 5 days at 4200 m and upon return to 1370 m after 4 weeks of altitude exposure (above 2500 m). The altitude exposure was interrupted by a decent to lower altitude where subjects spent two nights at 1370 m before returning to altitude again. Results: Ten subjects completed the NO3- supplementation. FMD (mean +/- SD) pre-trek value was 6.53 +/- 2.32% at 1370 m. At 3700 m FMD was reduced to 3.84 +/- 1.31% (p < 0.01) after PL supplementation but was normalized after receiving BJ (5.77 +/- 1.14% (p = 1.00). Eight of the subjects completed the interrupted 4-week altitude stay, and their FMD was lower at 4200 m (FMD 3.04 +/- 2.22%) and at post-altitude exposure to 1370 m (FMD 3.91 +/- 2.58%) compared to pre-trek FMD at 1370 m. Conclusion: Acute dietary NO3- supplementation may abolish altitude-induced reduction in endothelial function, and can serve as a dietary strategy to ensure peripheral vascular function in lowland subjects entering high altitude environments. (C) 2015 Elsevier Inc. All rights reserved.
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| 3. |
- Bueno, Emilio, et al.
(författare)
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Disparate response to microoxia and nitrogen oxides of the Bradyrhizobium japonicum napEDABC, nirK and norCBQD denitrification genes
- 2017
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Ingår i: Nitric oxide. - : Elsevier. - 1089-8603 .- 1089-8611. ; 68, s. 137-149
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Tidskriftsartikel (refereegranskat)abstract
- Expression of the Bradyrhizobium japonicum napEDABC, nirK and norCBQD denitrification genes requires low oxygen (O-2) tension and nitrate (NO3), through a regulatory network comprised of two coordinated cascades, FixLJ-FixK(2)-NnrR and RegSR-NifA. To precisely understand how these signals are integrated in the FixLJ-FixK(2)-NnrR circuit, we analyzed beta-Galactosidase activities from napE-lacZ, nirK-lacZ and norC-lacZ fusions, and performed analyses of NapC and NorC levels as well as periplasmic nitrate reductase (Nap) activity, in B. japonicum wildtype and fixK(2) and nnrR mutant backgrounds. While microoxic conditions (2% O-2 at headspace) were sufficient to induce expression of napEDABC and nirK genes and this control depends on FixK(2), norCBQD expression requires, in addition to microoxia, nitric oxide gas (NO) and both FixK(2) and NnrR transcription factors. Purified FixK(2) protein directly interacted and activated transcription in collaboration with B. japonicum RNA polymerase (RNAP) from the napEDABC and nirK promoters, but not from the norCBQD promoter. Further, recombinant NnrR protein bound exclusively to the norCBQD promoter in an O-2-sensitive manner. Our work suggest a disparate regulation of B. japonicum denitrifying genes expression with regard to their dependency to microoxia, nitrogen oxides (NOx), and the regulatory proteins FixK(2) and NnrR. In this control, expression of napEDABC and nirK genes requires microoxic conditions and directly depends on FixK2, while expression of norCBQD genes relies on NO, being NnrR the candidate which directly interacts with the norCBQD promoter.
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| 4. |
- Carlström, Mattias, et al.
(författare)
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Peritoneal dialysis impairs nitric oxide homeostasis and may predispose infants with low systolic blood pressure to cerebral ischemia
- 2016
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Ingår i: Nitric Oxide - Biology and Chemistry. - : Elsevier BV. - 1089-8603 .- 1089-8611. ; 58, s. 1-9
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Tidskriftsartikel (refereegranskat)abstract
- Background & purpose Infants on chronic peritoneal dialysis (PD) have an increased risk of developing neurological morbidities; however, the underlying biological mechanisms are poorly understood. In this clinical study, we investigated whether PD-mediated impairment of nitric oxide (NO) bioavailability and signaling, in patients with persistently low systolic blood pressure (SBP), can explain the occurrence of cerebral ischemia. Methods & results Repeated blood pressure measurements, serial neuroimaging studies, and investigations of systemic nitrate and nitrite levels, as well as NO signaling, were performed in ten pediatric patients on PD. We consistently observed the loss of both inorganic nitrate (-17 ± 3%, P < 0.05) and nitrite (-34 ± 4%, P < 0.05) during PD, which may result in impairment of the nitrate-nitrite-NO pathway. Indeed, PD was associated with significant reduction of cyclic guanosine monophosphate levels (-59.4 ± 15%, P < 0.05). This reduction in NO signaling was partly prevented by using a commercially available PD solution supplemented with l-arginine. Although PD compromised nitrate-nitrite-NO signaling in all cases, only infants with persistently low SBP developed ischemic cerebral complications. Conclusions Our data suggests that PD impairs NO homeostasis and predisposes infants with persistently low SBP to cerebral ischemia. These findings improve current understanding of the pathogenesis of infantile cerebral ischemia induced by PD and may lead to the new treatment strategies to reduce neurological morbidities.
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| 5. |
- Díaz, Miguel, Högskoleadjunkt, et al.
(författare)
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Differential effects of resveratrol on the dilator responses of femoral arteries, ex vivo
- 2019
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Ingår i: Nitric oxide. - : Elsevier. - 1089-8603 .- 1089-8611. ; 92, s. 1-10
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Tidskriftsartikel (refereegranskat)abstract
- Resveratrol is a plant-derived phytoalexin with antioxidant, anti-inflammatory and cardio-protective properties and may be a promising therapeutic intervention strategy in cardiovascular disease. Here, we investigated the acute direct effects of trans-resveratrol (RV), on acetylcholine (ACh)-induced and flow-mediated dilation (FMD) of isolated pressurized femoral arteries of young (4-month-old) and old (26-month-old) mice. Vessel exposure to RV enhanced ACh (0.01-1.0 mM)-induced dilation (p < 0.05), but not FMD (@ 5-10 μL⋅min-1) (p < 0.05) in both young and old mice. After RV incubation, acute nitric oxide (NO) production by cultured endothelial cells was increased in response to 0.01 mM ACh, but reduced by flow (5-10 μL⋅min-1; p < 0.05). In isolated femoral arteries from endothelial nitric oxide synthase knockout (eNOS-/-) mice, RV had no overall effect on flow mediated dilation, but potentiated ACh induced dilation, that was completely abolished by potassium channel blockers, Apamin and Tram 34 (p < 0.01). We demonstrate that the non-metabolised form of RV stimulates ACh-induced dilation via the NO and EDHF pathways, but not FMD by interaction with the cyclo-oxygenase pathway. Our findings have important implications in the use of RV (for both young and aged) under 'normal' non-diseased physiological states.
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| 7. |
- Finnerty, N., et al.
(författare)
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Increased brain nitric oxide levels following ethanol administration
- 2015
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Ingår i: Nitric oxide. - : Elsevier BV. - 1089-8603 .- 1089-8611. ; 47, s. 52-57
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Tidskriftsartikel (refereegranskat)abstract
- Nitric oxide is a ubiquitous messenger molecule, which at elevated concentrations has been implicated in the pathogenesis of several neurological disorders. Its role in oxidative stress, attributed in particular to the formation of peroxynitrite, proceeds through its high affinity for the superoxide radical. Alcoholism has recently been associated with the induction of oxidative stress, which is generally defined as a shift in equilibrium between pro-oxidant and anti-oxidant species in the direction of the former. Furthermore, its primary metabolite acetaldehyde, has been extensively associated with oxidative damage related toxic effects following alcohol ingestion. The principal objective of this study was the application of long term in vivo electrochemistry (LIVE) to investigate the effect of ethanol (0.125, 0.5 and 2.0 g kg-1) and acetaldehyde (12.5, 50 and 200 mg kg-1) on NO levels in the nucleus accumbens of freely moving rats. Systemic administrations of ethanol and acetaldehyde resulted in a dose-dependent increases in NO levels, albeit with very differing time courses. Subsequent to this the effect on accumbal NO levels, of subjecting the animal to different drug combinations, was also elucidated. The nitric oxide synthase inhibitor L-NAME (20 mg kg-1) and acetaldehyde sequestering agent D-penicillamine (50 mg kg-1) both attenuated the increase in NO levels following ethanol (1 g kg-1) administration. Conversely, the alcohol dehydrogenase inhibitor 4-methylpyrazole (25 mg kg-1) and catalase inhibitor sodium azide (10 mg kg-1) potentiated the increase in NO levels following ethanol administration. Finally, dual inhibition of aldehyde dehydrogenase and catalase by cyanamide (25 mg kg-1) caused an attenuation of ethanol effects on NO levels. Taken together these data highlight a robust increase in brain NO levels following systemic alcohol administration which is dependent on NO synthase activity and may involve both alcohol- and acetaldehyde-dependent mechanisms. © 2015 Elsevier Inc. All rights reserved.
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| 10. |
- Nybäck, Linn, et al.
(författare)
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Physiological and performance effects of nitrate supplementation during roller-skiing in normoxia and normobaric hypoxia
- 2017
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Ingår i: Nitric oxide. - : Elsevier BV. - 1089-8603 .- 1089-8611. ; 70, s. 1-8
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Tidskriftsartikel (refereegranskat)abstract
- The present study examined the effects of acute nitrate (NO3-) supplementation ingested in the form of concentrated beetroot juice on cross-country roller-ski performance in normoxia (N) and normobaric hypoxia (H). Eight competitive cross-country skiers (five males: age 22 ± 3 years, V·O2max 71.5 ± 4.7 mL kg-1·min-1; three females: age 21 ± 1 years, V·O2max 58.4 ± 2.5 mL kg-1·min-1) were supplemented with a single dose of NO3--rich beetroot juice (BRJ, ∼13 mmol NO3-) or a NO3--depleted placebo (PL, ∼0 mmol NO3-) and performed 2 x 6-min submaximal exercise bouts and a 1000-m time-trial (TT) on a treadmill in N (20.9% O2) or H (16.8% O2). The four experimental trials were presented in a randomised, counter-balanced order. Plasma NO3- and nitrite concentrations were significantly higher following BRJ compared to PL (both p < 0.001). However, respiratory variables, heart rate, blood lactate concentration, ratings of perceived exertion, and near-infrared spectroscopy-derived measures of muscle tissue oxygenation during submaximal exercise were not significantly different between BRJ and PL (all p > 0.05). Likewise, time to complete the TT was unaffected by supplementation in both N and H (p > 0.05). In conclusion, an acute dose of ∼13 mmol NO3- does not affect physiological or performance responses to submaximal or maximal treadmill roller-skiing in competitive cross-country skiers exercising in N and H.
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| 14. |
- Thornadtsson, Alexandra, 1988-, et al.
(författare)
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Altered levels of exhaled nitric oxide in rheumatoid arthritis
- 2018
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Ingår i: Nitric oxide. - : ACADEMIC PRESS INC ELSEVIER SCIENCE. - 1089-8603 .- 1089-8611. ; 76, s. 1-5
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Tidskriftsartikel (refereegranskat)abstract
- Background: Rheumatoid arthritis (RA) is an autoimmune disorder characterized by bone and joint destruction, but other organ systems can also be involved. Recent studies have suggested that the disease may start in the lungs. Exhaled nitric oxide (FENO) is a marker of inflammation. The aims of the study were to compare the NO parameters between subjects with RA and healthy control subjects, and to examine whether the NO parameters correlated with lung function and disease activity in the subjects with RA. Methods: Subjects with RA (n = 35) were recruited during their regular outpatient visits to the rheumatology department. The nitric oxide (NO) parameters: alveolar NO concentration (CANO), airway compartment diffusing capacity of NO (DawNO), and tissue concentration of NO in the airway wall (CawNO), were algorithmically estimated. Healthy subjects (n = 35) matched by age, gender and height were used as controls. Data are given in median, (quartile 25, 75). Wilcoxon Matched Pairs test was used for group comparisons. Mann-Whitney U test was used to make comparisons between any two groups and for pairwise comparisons. Correlations were tested with Spearman rank order correlation. Results: CANO was significantly lower in the RA subjects compared with healthy subjects; 1.1 (0.5, 1.8) ppb versus 2.4 (2.0, 3.0) ppb, (p < 0.001). CawNO was significantly lower in the RA subjects with 51 (22, 87) ppb versus 120 (76, 162) ppb in the control group. DaWNO was significantly higher at 25 (15, 36) mL/s in the RA group versus the control group's 7.7 (5.3, 10.7) mL/s. Conclusions: There are significant differences between subjects with RA and matched healthy control subjects regarding the exhaled NO parameters. It is unclear if this can be explained by the pathogenesis of RA, consequences of long-term disease, and/or due to drug treatment.
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