Ethyl nitrite is produced in the human stomach from dietary nitrate and ethanol, releasing nitric oxide at physiological pH: potential impact on gastric motility

2015 ◽  
Vol 82 ◽  
pp. 160-166 ◽  
Author(s):  
Bárbara S. Rocha ◽  
Bruno Gago ◽  
Rui M. Barbosa ◽  
Carlos Cavaleiro ◽  
João Laranjinha
Keyword(s):  
Nitric Oxide ◽  
Gastric Motility ◽  
Human Stomach ◽  
Dietary Nitrate ◽  
Potential Impact ◽  
Ethyl Nitrite

Intraluminal generation of nitric oxide from dietary nitrate is maximal at the gastro-oesophageal junction

2001 ◽  
Vol 120 (5) ◽  
pp. A245-A245
Author(s):  
E HENY ◽  
K IIJIMA ◽  
A MORIYA ◽  
K MCELROY ◽  
J GRANT ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Dietary Nitrate

scholarly journals Acute beetroot juice supplementation on sympathetic nerve activity: a randomized, double-blind, placebo-controlled proof-of-concept study

2017 ◽  
Vol 313 (1) ◽  
pp. H59-H65 ◽  
Author(s):  
Karambir Notay ◽  
Anthony V. Incognito ◽  
Philip J. Millar
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Sympathetic Outflow ◽  
Beetroot Juice ◽  
Proof Of Concept ◽  
Burst Frequency ◽  
Double Blind ◽  
Dietary Nitrate ◽  
Nitrate Supplementation ◽  
Central Sympathetic Outflow

Acute dietary nitrate ([Formula: see text]) supplementation reduces resting blood pressure in healthy normotensives. This response has been attributed to increased nitric oxide bioavailability and peripheral vasodilation, although nitric oxide also tonically inhibits central sympathetic outflow. We hypothesized that acute dietary [Formula: see text] supplementation using beetroot (BR) juice would reduce blood pressure and muscle sympathetic nerve activity (MSNA) at rest and during exercise. Fourteen participants (7 men and 7 women, age: 25 ± 10 yr) underwent blood pressure and MSNA measurements before and after (165–180 min) ingestion of 70ml high-[Formula: see text] (~6.4 mmol [Formula: see text]) BR or [Formula: see text]-depleted BR placebo (PL; ~0.0055 mmol [Formula: see text]) in a double-blind, randomized, crossover design. Blood pressure and MSNA were also collected during 2 min of static handgrip (30% maximal voluntary contraction). The changes in resting MSNA burst frequency (−3 ± 5 vs. 3 ± 4 bursts/min, P = 0.001) and burst incidence (−4 ± 7 vs. 4 ± 5 bursts/100 heart beats, P = 0.002) were lower after BR versus PL, whereas systolic blood pressure (−1 ± 5 vs. 2 ± 5 mmHg, P = 0.30) and diastolic blood pressure (4 ± 5 vs. 5 ± 7 mmHg, P = 0.68) as well as spontaneous arterial sympathetic baroreflex sensitivity ( P = 0.95) were not different. During static handgrip, the change in MSNA burst incidence (1 ± 8 vs. 8 ± 9 bursts/100 heart beats, P = 0.04) was lower after BR versus PL, whereas MSNA burst frequency (6 ± 6 vs. 11 ± 10 bursts/min, P = 0.11) as well as systolic blood pressure (11 ± 7 vs. 12 ± 8 mmHg, P = 0.94) and diastolic blood pressure (11 ± 4 vs. 11 ± 4 mmHg, P = 0.60) were not different. Collectively, these data provide proof of principle that acute BR supplementation can decrease central sympathetic outflow at rest and during exercise. Dietary [Formula: see text] supplementation may represent a novel intervention to target exaggerated sympathetic outflow in clinical populations. NEW & NOTEWORTHY The hemodynamic benefits of dietary nitrate supplementation have been attributed to nitric oxide-mediated peripheral vasodilation. Here, we provide proof of concept that acute dietary nitrate supplementation using beetroot juice can decrease muscle sympathetic outflow at rest and during exercise in a normotensive population. These results have applications for targeting central sympathetic overactivation in disease.

scholarly journals Role of Oral and Gut Microbiota in Dietary Nitrate Metabolism and Its Impact on Sports Performance

Nutrients ◽  
2020 ◽  
Vol 12 (12) ◽  
pp. 3611
Author(s):  
Rocío González-Soltero ◽  
María Bailén ◽  
Beatriz de Lucas ◽  
Maria Isabel Ramírez-Goercke ◽  
Helios Pareja-Galeano ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Gut Microbiota ◽  
Oral Bacteria ◽  
The Body ◽  
Sports Performance ◽  
Dietary Nitrate ◽  
Dietary Strategy ◽  
Nitrate Metabolism ◽  
Nitrate Supplementation

Nitrate supplementation is an effective, evidence-based dietary strategy for enhancing sports performance. The effects of dietary nitrate seem to be mediated by the ability of oral bacteria to reduce nitrate to nitrite, thus increasing the levels of nitrite in circulation that may be further reduced to nitric oxide in the body. The gut microbiota has been recently implicated in sports performance by improving muscle function through the supply of certain metabolites. In this line, skeletal muscle can also serve as a reservoir of nitrate. Here we review the bacteria of the oral cavity involved in the reduction of nitrate to nitrite and the possible changes induced by nitrite and their effect on gastrointestinal balance and gut microbiota homeostasis. The potential role of gut bacteria in the reduction of nitrate to nitrite and as a supplier of the signaling molecule nitric oxide to the blood circulation and muscles has not been explored in any great detail.

Relaxin counteracts the altered gastric motility of dystrophic (mdx) mice: functional and immunohistochemical evidence for the involvement of nitric oxide

2011 ◽  
Vol 300 (2) ◽  
pp. E380-E391 ◽  
Author(s):  
M. G. Vannucchi ◽  
R. Garella ◽  
G. Cipriani ◽  
M. C. Baccari
Keyword(s):  
Nitric Oxide ◽  
Gastric Motility ◽  
Electrical Field Stimulation ◽  
Gastric Fundus ◽  
Mdx Mice ◽  
No Production ◽  
Contractile Responses ◽  
Lower Amplitude ◽  
Immunohistochemical Evidence ◽  
Excitatory Responses

Impaired gastric motility ascribable to a defective nitric oxide (NO) production has been reported in dystrophic (mdx) mice. Since relaxin upregulates NO biosynthesis, its effects on the motor responses and NO synthase (NOS) expression in the gastric fundus of mdx mice were investigated. Mechanical responses of gastric strips were recorded via force displacement transducers. Evaluation of the three NOS isoforms was performed by immunohistochemistry and Western blot. Wild-type (WT) and mdx mice were distributed into three groups: untreated, relaxin pretreated, and vehicle pretreated. In strips from both untreated and vehicle-pretreated animals, electrical field stimulation (EFS) elicited contractile responses that were greater in mdx than in WT mice. In carbachol-precontracted strips, EFS induced fast relaxant responses that had a lower amplitude in mdx than in WT mice. Only in the mdx mice did relaxin depress the amplitude of the neurally induced excitatory responses and increase that of the inhibitory ones. In the presence of l-NNA, relaxin was ineffective. In relaxin-pretreated mdx mice, the amplitude of the EFS-induced contractile responses was decreased and that of the fast relaxant ones was increased compared with untreated mdx animals. Responses to methacholine or papaverine did not differ among preparations and were not influenced by relaxin. Immunohistochemistry and Western blotting showed a significant decrease in neuronal NOS expression and content in mdx compared with WT mice, which was recovered in the relaxin-pretreated mdx mice. The results suggest that relaxin is able to counteract the altered contractile and relaxant responses in the gastric fundus of mdx mice by upregulating nNOS expression.

Stationary flames of methyl nitrate and methyl nitrite

1955 ◽  
Vol 232 (1190) ◽  
pp. 389-403 ◽  
Keyword(s):  
Nitric Oxide ◽  
Atmospheric Pressure ◽  
Burning Velocity ◽  
Vapour Phase ◽  
Main Reaction ◽  
Methyl Nitrite ◽  
Nitrate Esters ◽  
Methyl Nitrate ◽  
Low Pressures ◽  
Ethyl Nitrite

Methyl nitrate (CH 3 ONO 2 ) is the most explosive of the nitrate esters, and previous studies have been confined mainly to the slow thermal decomposition, and to the vapour phase explosion at low pressures in closed vessels. A stationary decomposition flame has now been maintained and studied spectrographically. A t low pressures the zones of reaction are clearly separated. From the early stages of the flame strong formaldehyde bands are emitted. This decomposition flame has been successfully simulated in artificial mixtures of methyl nitrite with oxygen. The results obtained are in accord with the preliminary fission of the nitrate molecule in the pre-heat zone of the flame: CH 3 ONO 2 →CH 3 O + NO 2 . The combustion flame of m ethyl nitrate with oxygen, nitric oxide and nitrogen dioxide has also been examined at low pressures. At atmospheric pressure, m ethyl nitrite (CH 3 ONO) has been found to support a decomposition flame of very small burning velocity. However, the combustion of m ethyl nitrite with oxygen at atmospheric pressure is an extremely fast and vigorous flame. It has been observed in both pre-mixed and diffusion systems and information about the changes occurring in it have been obtained by absorption and emission spectroscopy. All the experimental results may be interpreted in terms of two general principles: the reluctance of nitric oxide to react except at high temperatures and pressures and the frequent occurrence in flames of extensive pyrolytic reactions before the main reaction zone is reached.

New insights into the regulation of inducible nitric oxide synthesis

1994 ◽  
Vol 266 (6) ◽  
pp. E829-E839 ◽  
Author(s):  
S. M. Morris ◽  
T. R. Billiar
Keyword(s):  
Nitric Oxide ◽  
Amino Acid ◽  
Host Response ◽  
Cell Types ◽  
Nitric Oxide Synthesis ◽  
Arginine Metabolism ◽  
Anatomic Site ◽  
Nitrogen Donor ◽  
Potential Impact ◽  
Inducible Nitric Oxide

Recent studies have identified the induction of nitric oxide (NO) synthesis in many cell types as part of the host response to sepsis and inflammation. Induced NO can have a variety of effects which may be detrimental or beneficial during sepsis or inflammation, depending on amount, duration, and anatomic site of synthesis. As arginine is the only physiological nitrogen donor for NO synthesis, metabolism of this amino acid may play an important role in regulation of NO synthesis during sepsis. This review will discuss the roles NO plays in sepsis and the potential impact of arginine metabolism on NO synthesis.

The effect of dietary nitrate supplement on exhaled nitric oxide

2017 ◽  
Vol 129 ◽  
pp. 382
Author(s):  
Juliet L. Kroll ◽  
Chelsey A. Werchan ◽  
Kylie M. Barfield ◽  
Thomas Ritz
Keyword(s):  
Nitric Oxide ◽  
Exhaled Nitric Oxide ◽  
Dietary Nitrate
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