The L-Arginine:Nitric Oxide Pathway Is the Major Source of Plasma Nitrite in Fasted Humans

1995 ◽  
Vol 211 (2) ◽  
pp. 705 ◽  
Author(s):  
P.M. Rhodes ◽  
A.M. Leone ◽  
P.L. Francis ◽  
A.D. Struthers ◽  
S. Moncada ◽  
...  
Keyword(s):  
Plasma Nitrite

Effects of Early Neuronal and Delayed Inducible Nitric Oxide Synthase Blockade on Cardiovascular, Renal, and Hepatic Function in Ovine Sepsis

2010 ◽  
Vol 113 (6) ◽  
pp. 1376-1384 ◽  
Author(s):  
Matthias Lange ◽  
Atsumori Hamahata ◽  
Daniel L. Traber ◽  
Yoshimitsu Nakano ◽  
Aimalohi Esechie ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Inducible Nitric Oxide Synthase ◽  
Nitric Oxide Synthase Inhibitor ◽  
Nitrite Nitrate ◽  
Synthase Inhibitor ◽  
Plasma Nitrite ◽  
Oxide Synthase ◽  
Organ Dysfunctions ◽  
Inducible Nitric Oxide

Background Recent evidence suggests that nitric oxide produced via the neuronal nitric oxide synthase is involved mainly in the early response to sepsis, whereas nitric oxide derived from the inducible nitric oxide synthase is responsible during the later phase. We hypothesized that early neuronal and delayed inducible nitric oxide synthase blockade attenuates multiple organ dysfunctions during sepsis. Methods Sheep were randomly allocated to sham-injured, nontreated animals (n = 6); injured (48 breaths of cotton smoke and instillation of Pseudomonas aeruginosa into the lungs), nontreated animals (n = 7); and injured animals treated with a neuronal nitric oxide synthase inhibitor from 1 to 12 h and an inducible nitric oxide synthase inhibitor from 12 to 24 h postinjury (n = 6). Results The injury induced arterial hypotension, vascular leakage, myocardial depression, and signs of renal and hepatic dysfunctions. The treatment significantly attenuated, but did not fully prevent, the decreases in mean arterial pressure and left ventricular stroke work index. Although the elevation of creatinine levels was partially prevented, the decreases in urine output and creatinine clearance were not affected. The injury-related increases in bilirubin levels, international normalized ratio, and lipid peroxidation in liver tissue were significantly attenuated. Although plasma nitrite/nitrate levels were significantly increased versus baseline from 12-24 h in controls, plasma nitrite/nitrate levels were not increased in treated animals. Conclusions The combination treatment shows potential benefit on sepsis-related arterial hypotension and surrogate parameters of organ dysfunctions in sheep. It may be crucial to identify the time course of expression and activation of different nitric oxide synthase isoforms in future investigations.

scholarly journals Contrasting effects of intervention with ETA and ETB receptor antagonists in hypertension induced by angiotensin II and high-salt dietThis article is one of a selection of papers published in the two-part special issue entitled 20 Years of Endothelin Research.

2010 ◽  
Vol 88 (8) ◽  
pp. 802-807 ◽  
Author(s):  
Erika I. Boesen ◽  
Jennifer S. Pollock ◽  
David M. Pollock
Keyword(s):  
Angiotensin Ii ◽  
Creatinine Clearance ◽  
Nitrate Concentration ◽  
Therapeutic Approaches ◽  
Receptor Antagonists ◽  
Induced Hypertension ◽  
Etb Receptor ◽  
Nitrite Nitrate ◽  
Plasma Nitrite ◽  
Selection Of

Endothelin (ET) receptor antagonists are antihypertensive and renoprotective in angiotensin II (AngII)-induced hypertension if administered when AngII infusion commences, but their effects on established hypertension are poorly understood. We therefore tested the effects of intervening with an ETA (ABT-627) or ETB (A-192621) receptor antagonist after establishing hypertension with AngII (65 ng/min s.c.) plus 8% NaCl diet (AngII–HS) in rats. Prior to administration of ABT-627, AngII–HS and AngII–HS plus ABT-627 groups displayed robust hypertension (mean arterial pressure (MAP), 170 ± 5 and 165 ± 5 mm Hg versus 110 ± 3 mm Hg in normal salt control rats at day 7, P < 0.05). Administering ABT-627 from day 8 of AngII–HS treatment prevented further rises in MAP (168 ± 5 and 191 ± 3 mm Hg at day 13 in AngII–HS plus ABT-627 and AngII–HS, P < 0.001), without blunting the significant increases in urinary protein (19-fold), albumin (25-fold), or MCP-1 excretion (6- to 8-fold) or the reduction in creatinine clearance. Administering A-192621 from day 8 mildly exacerbated AngII–HS induced hypertension (P < 0.05 for AngII–HS versus AngII–HS plus A-192621 on days 11 and 12 only) and reduced plasma nitrite/nitrate concentration (P < 0.05), without affecting proteinuria, albuminuria, or creatinine clearance. These results confirm the importance of ETA receptor signaling in maintaining AngII–HS hypertension and suggest that including ETB receptor blockade in therapeutic approaches to treating hypertension would be ineffective or even counterproductive.

A simple, fast and inexpensive automated technique for measurement of plasma nitrite

2010 ◽  
Vol 48 (12) ◽  
Author(s):  
Renata da Silva Pereira ◽  
Sílvia Juliane Piva ◽  
Etiane Tatsch ◽  
Helena Kober ◽  
Patrícia Gomes ◽  
...  
Keyword(s):  
Automated Technique ◽  
Plasma Nitrite

scholarly journals Plasma nitrite response and arterial reactivity differentiate vascular health and performance

Nitric Oxide ◽  
2009 ◽  
Vol 20 (4) ◽  
pp. 231-237 ◽  
Author(s):  
Jason D. Allen ◽  
Elizabeth M. Miller ◽  
Earl Schwark ◽  
Jennifer L. Robbins ◽  
Brian D. Duscha ◽  
...  
Keyword(s):  
Vascular Health ◽  
Arterial Reactivity ◽  
And Performance ◽  
Plasma Nitrite

scholarly journals Nitrite Intoxication of Common Carp (Cyprinus carpio L.) at Different Water Temperatures

2006 ◽  
Vol 75 (4) ◽  
pp. 561-569 ◽  
Author(s):  
H. Kroupová ◽  
J. Máchová ◽  
V. Piačková ◽  
M. Flajšhans ◽  
Z. Svobodová ◽  
...  
Keyword(s):  
Blood Plasma ◽  
Common Carp ◽  
Cyprinus Carpio ◽  
Haemoglobin Concentration ◽  
Nitrite Accumulation ◽  
Corpuscular Haemoglobin ◽  
Mean Corpuscular Haemoglobin ◽  
Higher Temperature ◽  
Lower Temperature ◽  
Plasma Nitrite

Common carp (Cyprinus carpio L.) were exposed to nitrite (1.45 mmol l-1 NO2-) for 48 hours at 14 °C and 20 °C, in order to investigate the mechanism of nitrite poisoning at these water temperatures. The effect of nitrite exposure on fish was assessed on selected haematological and biochemical indicators of the blood. Moreover, nitrite accumulation in the blood, liver and muscle was measured. Nitrite exposure produced high levels of methaemoglobin (88.2 ± 3.3% and 92.9 ± 6.1%) at both water temperatures compared with controls (0.3 ± 0.6% and 2.6 ± 3.0%). High fish mortality occurred in experimental groups (30% and 51%) compared with controls (0%). Nitrite exposure also resulted in an accumulation of nitrite in the fish body. The highest nitrite levels developed in the blood plasma, followed by the liver and muscle, respectively. Carp concentrated nitrite in the blood plasma and tissues to markedly higher levels at higher temperature (20 °C). The plasma nitrite concentrations (10.5 ± 1.9 mmol l-1) were in this case more than 7 times higher than the environmental one. At lower temperature (14 °C), plasma nitrite concentration reached 5.0 ± 1.5 mmol l-1. In either event, plasma K+ levels increased and Cl- levels and osmolality remained unchanged. Plasma Na+ levels slightly decreased at the higher temperature. Nitriteexposed fish showed lower haematocrit values (PCV) at both experimental temperatures compared with controls. At 20 °C, the blood haematocrit decrease (0.20 ± 0.02 l l-1) was accompanied by a low erythrocyte count (1.05 ± 0.12 1012 l-1) and by a low haemoglobin level (51 ± 11 g l-1). At the lower temperature (14 °C), the haematocrit decrease (0.25 ± 0.02 l l-1) was caused by a low mean corpuscular volume (167 ± 27 fl). No significant changes were observed in the mean corpuscular haemoglobin (MCH), mean corpuscular haemoglobin concentration (MCHC), or selected erythrocyte dimensions (major axis, minor axis and aspect ratio).

scholarly journals Comodulation of NO-Dependent Vasodilation by Erythroid Band 3 and Hemoglobin: A GP.Mur Athlete Study

2021 ◽  
Vol 8 ◽  
Author(s):  
Kate Hsu ◽  
Yen-Yu Liu ◽  
Wei-Chin Tseng ◽  
Kuang-Tse Huang ◽  
Chia-Yuan Liu ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Arterial Occlusion ◽  
Band 3 ◽  
Flow Mediated Dilation ◽  
Red Cell Membrane ◽  
Anion Exchanger 1 ◽  
Before And After ◽  
Dependent Flow ◽  
Plasma Nitrite

GP.Mur, a red blood cell (RBC) hybrid protein encoded by glycophorin B-A-B, increases expression of erythroid band 3 (Anion Exchanger-1, SLC4A1). GP.Mur is extremely rare but has a prevalence of 1–10% in regions of Southeast Asia. We unexpectedly found slightly higher blood pressure (BP) among healthy Taiwanese adults with GP.Mur. Since band 3 has been suggested to interact with hemoglobin (Hb) to modulate nitric oxide (NO)-dependent hypoxic vasodilation during the respiratory cycle, we hypothesized that GP.Mur red cells could exert differentiable effects on vascular tone. Here we recruited GP.Mur-positive and GP.Mur-negative elite male college athletes, as well as age-matched, GP.Mur-negative non-athletes, for NO-dependent flow-mediated dilation (FMD) and NO-independent dilation (NID). The subjects were also tested for plasma nitrite and nitrate before and after arterial occlusion in FMD. GP.Mur+ and non-GP.Mur athletes exhibited similar heart rates and blood pressure, but GP.Mur+ athletes showed significantly lower FMD (4.8 ± 2.4%) than non-GP.Mur athletes (6.5 ± 2.1%). NO-independent vasodilation was not affected by GP.Mur. As Hb controls intravascular NO bioavailability, we examined the effect of Hb on limiting FMD and found it to be significantly stronger in GP.Mur+ subjects. Biochemically, plasma nitrite levels were directly proportional to individual band 3 expression on the red cell membrane. The increase of plasma nitrite triggered by arterial occlusion also showed small dependency on band 3 levels in non-GP.Mur subjects. By the GP.Mur comparative study, we unveiled comodulation of NO-dependent vasodilation by band 3 and Hb, and verified the long-pending role of erythroid band 3 in this process.

scholarly journals Impaired vasoreactivity despite an increase in plasma nitrite in patients with abdominal aortic aneurysms

2002 ◽  
Vol 35 (2) ◽  
pp. 363-367 ◽  
Author(s):  
Brian S. Knipp ◽  
David A. Peterson ◽  
Sanjay Rajagopalan ◽  
Christine Kehrer ◽  
John W. Ford ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysms ◽  
Aortic Aneurysms ◽  
Abdominal Aortic ◽  
Plasma Nitrite

Nitric Oxide Mediates Hepatic Cytochrome P450 Dysfunction Induced by Endotoxin

1996 ◽  
Vol 84 (6) ◽  
pp. 1435-1442 ◽  
Author(s):  
Claudia M. Muller ◽  
Annette Scierka ◽  
Richard L. Stiller ◽  
Yong-Myeong Kim ◽  
Ryan D. Cook ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cytochrome P450 ◽  
Drug Metabolism ◽  
Sprague Dawley ◽  
Cytochrome P450 Content ◽  
Nitrate Concentrations ◽  
Hypnotic Drugs ◽  
Plasma Nitrite

Background Animals subjected to immunostimulatory conditions (sepsis) exhibit decreased total cytochrome P450 content and decreased P450-dependent drug metabolism. Cytochrome P450 function is of clinical significance because it mediates the metabolism of some opioid and hypnotic drugs. The authors tested the hypothesis that reduced P450 function and decreased drug metabolism in sepsis are mediated by endotoxin-enhanced synthesis of nitric oxide. Methods Hepatic microsomes were prepared from male Sprague-Dawley rats in nontreated rats, rats pretreated with phenobarbital and rats receiving aminoguanidine or NG-L-monomethyl-arginine alone. Nitric oxide synthesis was augmented for 12 h with a single injection of bacterial lipopolysaccharides. Nitric oxide synthase was inhibited with aminoguanidine or N(G)-L-monomethyl-arginine during the 12 h of endotoxemia in some animals. Plasma nitrite and nitrate concentrations were measured in vivo, and total microsomal P450 content, and metabolism of ethylmorphine and midazolam in vitro. Results Administration of endotoxin increased plasma nitrite and nitrate concentrations, decreased total cytochrome P450 content, and decreased metabolism of ethylmorphine and midazolam. Inhibition of nitric oxide formation by aminoguanidine or N(G)-L-monomethyl-arginine partially prevented the endotoxin-induced effects in the nontreated and phenobarbital-treated groups. Aminoguanidine or N(G)-L-monomethyl-arginine alone did not have an effect on either total cytochrome P450 content or P450-dependent drug metabolism. Plasma nitrite and nitrate concentrations correlated significantly negatively with P450 content (nontreated r = -0.88, phenobarbital r = -0.91), concentrations of formed formaldehyde (nontreated r = -0.87, phenobarbital r = -0.95), and concentrations of midazolam metabolites (4-OH midazolam nontreated r = -0.88, phenobarbital r = -0.93, and 1'-OH midazolam nontreated r = -0.88, phenobarbital r = -0.97). Conclusions Altered hepatic microsomal ethylmorphine and midazolam metabolism during sepsis is mediated in large part by nitric oxide.

P168. Plasma nitrite reserve with exercise predicts age-related endothelial dysfunction in humans

Nitric Oxide ◽  
2006 ◽  
Vol 14 (4) ◽  
pp. 72
Author(s):  
Tienush Rassaf ◽  
Thomas Lauer ◽  
Christian Heiss ◽  
Jan Balzer ◽  
Petra Kleinbongard ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Age Related ◽  
Plasma Nitrite
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