scholarly journals Effect of Multicomponent Training on Blood Pressure, Nitric Oxide, Redox Status, and Physical Fitness in Older Adult Women: Influence of Endothelial Nitric Oxide Synthase (NOS3) Haplotypes

2017 ◽  
Vol 2017 ◽  
pp. 1-12 ◽  
Author(s):  
Atila Alexandre Trapé ◽  
Elisangela Aparecida da Silva Lizzi ◽  
Thiago Correa Porto Gonçalves ◽  
Jhennyfer Aline Lima Rodrigues ◽  
Simone Sakagute Tavares ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Physical Fitness ◽  
Older Adult ◽  
Elbow Flexion ◽  
Redox Status ◽  
Adult Women ◽  
Nitrite Concentration ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

The purpose of this study was to verify the influence of the genotype or haplotype (interaction) of the NOS3 polymorphisms [-786T>C, 894G>T (Glu298Asp), and intron 4b/a] on the response to multicomponent training (various capacities and motor skills) on blood pressure (BP), nitrite concentration, redox status, and physical fitness in older adult women. The sample consisted of 52 participants, who underwent body mass index and BP assessments. Physical fitness was evaluated by six-minute walk, elbow flexion, and sit and stand up tests. Plasma/blood samples were used to evaluate redox status, nitrite concentration, and genotyping. Associations were observed between isolated polymorphisms and the response of decreased systolic and diastolic BP and increased nitrite concentration and antioxidant activity. In the haplotype analysis, the group composed of ancestral alleles (H1) was the only one to present improvement in all variables studied (decrease in systolic and diastolic BP, improvement in nitrite concentration, redox status, and physical fitness), while the group composed of variant alleles (H8) only demonstrated improvement in some variables of redox status and physical fitness. These findings suggest that NOS3 polymorphisms and physical training are important interacting variables to consider in evaluating redox status, nitric oxide availability and production, and BP control.

scholarly journals NOS3 Polymorphisms Can Influence the Effect of Multicomponent Training on Blood Pressure, Nitrite Concentration and Physical Fitness in Prehypertensive and Hypertensive Older Adult Women

2021 ◽  
Vol 12 ◽  
Author(s):  
Átila Alexandre Trapé ◽  
Jhennyfer Aline Lima Rodrigues ◽  
Letícia Perticarrara Ferezin ◽  
Gustavo Duarte Ferrari ◽  
Elisangela Aparecida da Silva Lizzi ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Physical Fitness ◽  
Older Adult ◽  
Physical Training ◽  
Elbow Flexion ◽  
Training Intervention ◽  
Similar Response ◽  
Adult Women ◽  
Nitrite Concentration ◽  
Hypertensive Group

Associations of endothelial nitric oxide synthase (NOS3) polymorphisms with hypertension and response to exercise training in prehypertensive and hypertensive older adult women remain unclear. This study used a multicomponent program (various capacities and motor skills) in the physical training intervention. It analyzed the influence of NOS3 polymorphisms [−786T > C, 894G > T (Glu298Asp), and intron 4b/a] on the response of blood pressure (BP), nitrite concentration, and physical fitness in older adult women. Fifty-two participants aged between 50 and 80 underwent body mass index, BP, 6-min walk, elbow flexion, and sit and stand-up tests to assess physical fitness. The intervention duration was 12 weeks, twice a week, on non-consecutive days. Each session lasted 90 min, maintaining an intensity between 13 (moderate) and 15 (intense), controlled by the Subjective Effort Perception Scale. Plasma/blood samples were collected to assess nitrite concentration and genotyping. The statistical analysis included Fisher’s exact test and linear mixed-effects models. The multicomponent training’s positive effect was observed with a similar response in both prehypertensive and hypertensive groups. However, carriers of different genotypes demonstrated different responses to training: the decreases in systolic and diastolic BP and increases in nitrite expected from the physical training were smaller in variant genotype than ancestral genotype carriers, especially in the hypertensive group. At positions −786T > C and Glu298Asp, only the ancestral genotypes showed a decrease in diastolic BP (Δ% = −8.1, and Δ% = −6.5, respectively) and an increase on nitrite (Δ% = 19.1, and Δ% = 24.1, respectively) in the hypertensive group. Our results show that the benefits of a multicomponent training intervention seem to be genotype-dependent. It should be possible to consider genetic variants when selecting an exercise treatment intervention.

Abstract 111: Xanthine Oxidoreductase Plays a Key Role in Nitrate, Nitrite and Nitric Oxide Homeostasis When the Endothelial Nitric Oxide Synthase is Compromised

Hypertension ◽  
2016 ◽  
Vol 68 (suppl_1) ◽  
Author(s):  
Maria Peleli ◽  
Christa Zollbrecht ◽  
Marcelo Montenegro ◽  
Michael Hezel ◽  
Eddie Weitzberg ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Primary Source ◽  
No Production ◽  
Xanthine Oxidoreductase ◽  
Physiological Conditions ◽  
Inorganic Nitrate ◽  
Nos Inhibitor ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Xanthine oxidoreductase (XOR) is generally known as a source of superoxide production, but this enzyme has also been suggested to mediate NO production via reduction of inorganic nitrate (NO 3 - ) and nitrite(NO 2 - ). This pathway for NO generation is of particular importance during certain pathologies, whereas endothelial NO synthase (eNOS) is the primary source of vascular NO generation under normal physiological conditions. The exact interplay between the NOS and XOR-derived NO is not yet fully elucidated. The aim of the present study was to investigate if eNOS deficiency is partly compensated by XOR upregulation and sensitization of the NO 3 - - NO 2 - - NO pathway. NO 3 - and NO 2 - were similar between naïve eNOS KO and wildtype (wt) mice, but reduced upon chronic treatment with the non-selective NOS inhibitor L-NAME (wt: 25.0±5.2, eNOS KO: 39.2±6.4, L-NAME: 8.2±1.6 μ NO 3 - -, wt: 0.38±0.07, eNOS KO: 0.42±0.04, L-NAME: 0.12±0.02 μ NO 2 - ). XOR function was upregulated in eNOS KO compared with wt mice [(mRNA: wt 1±0.07, eNOS KO 1.38±0.17), (activity: wt 825±54, eNOS KO 1327±280 CLU/mg/min), (uric acid: wt 32.87±1.53, eNOS KO 43.23±3.54 μ)]. None of these markers of XOR activity was increased in nNOS KO and iNOS KO mice. Following acute dose of NO 3 - (10 mg/kg bw, i.p.), the increase of plasma NO 2 - was more pronounced in eNOS KO (+0.51±0.13 μ) compared with wt (+0.22±0.09 μ), and this augmented response in the eNOS KO was abolished by treatment with the highly selective XOR inhibitor febuxostat (FEB). Liver from eNOS KO had higher reducing capacity of NO 2 - to NO compared with wt, and this effect was attenuated by FEB (Δppb of NO: wt +8.7±4.2, eNOS KO +44.2±15.0, wt+FEB +22.2±9.6, eNOS KO+FEB +26.8±10.2). Treatment with FEB increased blood pressure in eNOS KO (ΔMAP:+10.2±5.6 mmHg), but had no effect in wt (ΔMAP:-0.6±3.3 mmHg). Supplementation with NO 3 - (10 mM, drinking water) reduced blood pressure in eNOS KO (ΔMAP: -6.3±2.2 mmHg), and this effect was abolished by FEB (ΔMAP: +1.1±1.9 mmHg). In conclusion, upregulated and altered XOR function in conditions with eNOS deficiency can facilitate the NO 3 - - NO 2 - - NO pathway and hence play a significant role in vascular NO homeostasis.

Abstract 322: Acute Inhibition of GTP Cyclohydrolase 1 Uncouples Endothelial Nitric Oxide Synthase and Elevates Blood Pressure

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Shuangxi Wang ◽  
Jian Xu ◽  
Ping Song ◽  
Yong Wu ◽  
Junhua Zhang ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
De Novo ◽  
Gtp Cyclohydrolase ◽  
South Central ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Endothelium Dependent Relaxation

Objective: GTP cyclohydrolase 1 (GTPCH1) is the rate-limiting enzyme in de novo synthesis of tetrahydrobiopterin (BH4), an essential cofactor for endothelial nitric oxide synthase (eNOS) dictating at least partly, the balance of nitric oxide (NO) and superoxide (O 2 .− ) produced by this enzyme. The aim of this study is to determine the effects of acute inhibition of GTPCH1 on BH4, eNOS function, and blood pressure. Methods: The biopterin content was detected by HPLC. O 2 .− and NO productions were assayed by using DHE and DAF fluorescence respectively. The vessel relaxation was assayed by organ chamber. The blood pressure in wild-type (WT) or eNOS −/− mice was determined by a carotid catheter method. Results: Exposure of bovine or mouse aortic endothelial cells to GTPCH1 inhibitors (10 mM DAHP or 1 mM NAS) for 24 hours or GTPCH1 siRNA transfection significantly reduced both BH4 and NO levels, but increased O 2 .− levels. This increase was abolished by 10 μM L-sepiapterin (BH4 precursor) or 1 mM L-NAME (non-selective NOS inhibitor). Incubation of isolated WT mice aortas with DAHP or NAS for 24 hours impaired acetylcholine-induced endothelium-dependent relaxation, but not endothelium-independent relaxation. Aortas from GTPCH1 siRNA-injected mice, but not their control-siRNA injected mice, also exhibited impaired endothelium-dependent relaxation. Furthermore, GT-PCH1 siRNA injection in mice reduced BH4 levels in aortas, associated with increased aortic levels of O 2 .− , 3-nitrotyrosine, and adhesion molecules (ICAM1 and VCAM1). In addition, an elevated mean, systolic, and diastolic blood pressure was induced by GTPCH1 siRNA injection in vivo , but not control siRNA (mean blood pressure: 114.28±4.48 vs . 136.81±2.45 mmHg) in WT mice. GTPCH1 siRNA was unable to elicit the similar effects in eNOS −/− mice, including increased oxidative stress (O 2 .− , 3-nitrotyrosine, ICAM1, VCAM1) and blood pressure. Finally, sepiapterin supplementation, which had no effect on high blood pressure in eNOS −/− mice, partially reversed GTPCH1 siRNA-induced elevation of systemic blood pressure in WT mice. Conclusion: GTPCH1 via BH4 maintains normal blood pressure and endothelial function by preserving eNOS-dependent NO biosynthesis. This research has received full or partial funding support from the American Heart Association, AHA South Central Affiliate (Arkansas, New Mexico, Oklahoma & Texas).

scholarly journals The Effects of Oral l-Arginine and l-Citrulline Supplementation on Blood Pressure

Nutrients ◽  
2019 ◽  
Vol 11 (7) ◽  
pp. 1679 ◽  
Author(s):  
David Khalaf ◽  
Marcus Krüger ◽  
Markus Wehland ◽  
Manfred Infanger ◽  
Daniela Grimm
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Animal Studies ◽  
Current Data ◽  
No Production ◽  
First Pass Metabolism ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
Antihypertensive Properties ◽  
Pass Metabolism

Nitric oxide (NO) is a well-known vasodilator produced by the vascular endothelium via the enzyme endothelial nitric oxide synthase (eNOS). The inadequate production of NO has been linked to elevated blood pressure (BP) in both human and animal studies, and might be due to substrate inaccessibility. This review aimed to investigate whether oral administration of the amino acids l-arginine (Arg) and l-citrulline (Cit), which are potential substrates for eNOS, could effectively reduce BP by increasing NO production. Both Arg and Cit are effective at increasing plasma Arg. Cit is approximately twice as potent, which is most likely due to a lower first-pass metabolism. The current data suggest that oral Arg supplementation can lower BP by 5.39/2.66 mmHg, which is an effect that is comparable with diet changes and exercise implementation. The antihypertensive properties of Cit are more questionable, but are likely in the range of 4.1/2.08 to 7.54/3.77 mmHg. The exact mechanism by which Cit and Arg exert their effect is not fully understood, as normal plasma Arg concentration greatly exceeds the Michaelis constant (Km) of eNOS. Thus, elevated plasma Arg concentrations would not be expected to increase endogenous NO production significantly, but have nonetheless been observed in other studies. This phenomenon is known as the “l-arginine paradox”.

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