Biotransformation of Nitric Oxide

Yoshida, Kazuo; Kasama, Kazuo

doi:10.2307/3430611

Cited by 21 publications

(23 citation statements)

References 27 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Nitrite is also a source of NO z in the alimentary canal (96,97) ; it is largely the product of reduction by the oral biota of nitrate secreted by salivary glands (98) . Nitrite-derived NO z also kills bacteria in the stomach (99) ; in this acidic medium, nitrite reacts with free amino acids yielding N-nitroso-proline from arginine (100) , as well as N 2 as indicated above (84) . The 'obese' microbiota (101,102) is probably a consequence of this magnified effect of NO x (103) ; changes in the gut microbial ecosystem and composition also influence the relationships with the host through modulation of the immune response (104,105) .…”

Section: Nitrite and Other Forms Of Nitrogen Excretionmentioning

confidence: 99%

The problem of nitrogen disposal in the obese

Alemany

2012

Nutr. Res. Rev.

View full text Add to dashboard Cite

Amino-N is preserved because of the scarcity and nutritional importance of protein. Excretion requires its conversion to ammonia, later incorporated into urea. Under conditions of excess dietary energy, the body cannot easily dispose of the excess amino-N against the evolutively adapted schemes that prevent its wastage; thus ammonia and glutamine formation (and urea excretion) are decreased. High lipid (and energy) availability limits the utilisation of glucose, and high glucose spares the production of ammonium from amino acids, limiting the synthesis of glutamine and its utilisation by the intestine and kidney. The amino acid composition of the diet affects the production of ammonium depending on its composition and the individual amino acid catabolic pathways. Surplus amino acids enhance protein synthesis and growth, and the synthesis of non-protein-N-containing compounds. But these outlets are not enough; consequently, less-conventional mechanisms are activated, such as increased synthesis of NO z followed by higher nitrite (and nitrate) excretion and changes in the microbiota. There is also a significant production of N 2 gas, through unknown mechanisms. Health consequences of amino-N surplus are difficult to fathom because of the sparse data available, but it can be speculated that the effects may be negative, largely because the fundamental N homeostasis is stretched out of normalcy, forcing the N removal through pathways unprepared for that task. The unreliable results of hyperproteic diets, and part of the dysregulation found in the metabolic syndrome may be an unwanted consequence of this N disposal conflict.

show abstract

Section: Nitrite and Other Forms Of Nitrogen Excretionmentioning

confidence: 99%

The problem of nitrogen disposal in the obese

Alemany

2012

Nutr. Res. Rev.

View full text Add to dashboard Cite

show abstract

“…Within the body, NO 2 , and the produced nitrogen dioxide ion (NO 2 -), is thought to be involved in oxidative stress, injury of the cell membrane, impairment of the function of alveolar macrophages and epithelial cells (7), reaction with lung tissue, and hemoglobin in erythrocytes and result in various injuries, carcinogenesis, and aging (8). NO 2 increases lipid peroxide formation, inhibits antioxidative enzymes (9), and exerts profound physiological effects on the lung, the liver, the immune system, and, especially, blood vessels (2).…”

mentioning

confidence: 99%

Exposure to urban nitrogen dioxide pollution and the risk of myocardial infarction

Gražulevičienė¹,

Marozienė²,

Dulskienė³

et al. 2004

Scand J Work Environ Health

View full text Add to dashboard Cite

“…11 The NO produced is oxidized rapidly to the stable metabolites, NO 2 Ϫ ϩ NO 3 Ϫ (NO x ). 12 Recently, Sessa et al 13 reported that increased endothelial shear stress by chronic exercise increases NO production (NO x ) and eNOS gene expression in the coronary arteries and aorta of normal dogs. The increased synthesis of NO is a normal chronic adaptive mechanism of the endothelium in response to a chronic increase in shear stress.…”

mentioning

confidence: 99%

Enhanced Release of Nitric Oxide in Response to Changes in Flow and Shear Stress in the Superior Mesenteric Arteries of Portal Hypertensive Rats

1998

View full text Add to dashboard Cite

Increased nitric oxide (NO) release has been implicated in the pathogenesis of the hyperdynamic circulation in portal hypertension. NOS 3 (eNOS) causes NO release from the endothelium in response to physical stimuli, such as increased blood flow and shear stress. We evaluated the functional activity of the endothelium in the superior mesenteric arterial bed of portal hypertensive rats through direct measurement of NO metabolites (NO x ) during changes in flow and shear stress. The in vitro perfusion system (McGregor) was used in sham and portal vein-ligated (PVL) rats. Shear stress was applied gradually to superior mesenteric arterial beds by increasing the perfusion rate. Flow studies were performed serially before and after incubation with either Krebs solution alone or with the NO-inhibitor, N G -monomethyl-L-arginine (L-NMMA). NO x concentrations in the perfusate were measured using chemiluminescence. The slope of NO x release versus flow-induced shear stress was calculated. Before L-NMMA administration, NO x concentrations and release of NO in PVL rats were significantly elevated in comparison with sham rats at flow rates of 32, 40, and 48 mL/min. The slope of NO x production versus shear stress index was significantly higher in PVL than in sham rats. After L-NMMA incubation, the decrease in slope was significantly larger in PVL rats. This study provides direct evidences of an increased NO synthesis by the superior mesenteric arterial vascular endothelium of PVL animals in response to shear stress. The increased NO output in response to shear stress suggests an adaptative mechanism developed by the vascular endothelial cells in response to a chronic increase in flow-mediated shear stress. (HEPATOLOGY 1998;28:1467-1473.)Patients with cirrhosis 1 and animals with portal hypertension 2 are characterized by having a hyperdynamic circulation, especially in the splanchnic vessels. Splanchnic vasodilatation may arise from an excess production of vasodilatory substances, 3 which in turn leads to hyporeactivity to endogenous vasoconstrictors. 4 In studies using systemic administration of stereospecific nitric oxide synthase (NOS) inhibitors, increased synthesis of NO has been implicated in the pathogenesis of the hyperdynamic circulation in portal hypertension. 5,6 In clinical studies in patients with cirrhosis, increased NO production has been suggested by measurement of increased concentrations of NO metabolites in serum and urine. 7,8 Normally, NOS present in the vascular endothelium (NOS 3 or eNOS) produces NO transiently in response to physical stimuli, such as an increased blood flow and shear stress. 9,10 This is a unique function of eNOS. Flow-mediated vasodilatation is proportional to the shear stress induced by blood flow and independent of changes in luminal pressure. It is now recognized that this constitutive mechanism requires the integrity of the endothelium and in most conduit vessels is caused by the release of NO. This is the normal mechanism that mediates vascular dilatation secondary to increases...

show abstract

Biotransformation of Nitric Oxide

Cited by 21 publications

References 27 publications

The problem of nitrogen disposal in the obese

The problem of nitrogen disposal in the obese

Exposure to urban nitrogen dioxide pollution and the risk of myocardial infarction

Enhanced Release of Nitric Oxide in Response to Changes in Flow and Shear Stress in the Superior Mesenteric Arteries of Portal Hypertensive Rats

Contact Info

Product

Resources

About