Analysis of Plasma Nitrite/Nitrate in Human Thermal Injury.

2001 ◽  
Vol 194 (2) ◽  
pp. 129-136 ◽  
Author(s):  
Daizoh Saitoh ◽  
Akira Takasu ◽  
Kunitaro Fukuzuka ◽  
Hirohumi Norio ◽  
Toshihisa Sakamoto ◽  
...  
Keyword(s):  
Thermal Injury ◽  
Nitrite Nitrate ◽  
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.

Superoxide dismutase-3 promotes full expression of the EPO response to hypoxia

Blood ◽  
2004 ◽  
Vol 104 (1) ◽  
pp. 43-50 ◽  
Author(s):  
Hagir B. Suliman ◽  
Mervat Ali ◽  
Claude A. Piantadosi
Keyword(s):  
Superoxide Dismutase ◽  
Regulatory Element ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Adaptation To Hypoxia ◽  
Knock Out ◽  
Superoxide Dismutase 3 ◽  
Nitrite Nitrate ◽  
Plasma Nitrite ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Abstract Extracellular superoxide dismutase (SOD3) is the primary extracellular enzymatic scavenger of superoxide (\batchmode \documentclass[fleqn,10pt,legalpaper]{article} \usepackage{amssymb} \usepackage{amsfonts} \usepackage{amsmath} \pagestyle{empty} \begin{document} \(^{{\cdot}}\mathrm{O}_{2}^{-}\) \end{document}). SOD3's expression is highest in the kidney, but its distribution and biologic functions there are unknown. To investigate the function of renal SOD3, we colocalized it with erythropoietin (EPO) to proximal tubules using in situ hybridization and immunohistochemistry. We then exposed wild-type (Wt) and SOD3 knock-out (KO) mice to hypoxia and found a late hematocrit response in the KO strain. EPO mRNA expression was attenuated in KO mice during the first 6 hours of hypoxia preceded at 2 hours by less accumulation of nuclear hypoxia-inducible transcription factor 1 α (HIF-1α) protein. Meanwhile KO mice exposed to hypoxia showed increases in renal mRNA for superoxide-producing nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX4) and early significant increases in glutathione disulfide (GSSG)/glutathione (GSH), a marker of oxidative stress, compared with Wt mice. Plasma nitrite/nitrate and renal 3-nitrotyrosine (3-NTyr), indicating peroxynitrite formation, increased later in hypoxia, and renal endothelial nitric oxide synthase protein induction was similar in both strains. These data show that hypoxic activation of HIF-1α and its target gene EPO in mouse kidney is regulated closely by the oxidant/antioxidant equilibrium involving SOD3, thus identifying renal SOD3 as a regulatory element in the body's innate adaptation to hypoxia.

Correlation of plasma nitrite/nitrate levels and inducible nitric oxide gene expression among women with cervical abnormalities and cancer

Nitric Oxide ◽  
2016 ◽  
Vol 52 ◽  
pp. 21-28 ◽  
Author(s):  
A. Pavani Sowjanya ◽  
Meera Rao ◽  
Haripriya Vedantham ◽  
Basany Kalpana ◽  
Usha Rani Poli ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nitric Oxide ◽  
Nitrite Nitrate ◽  
Plasma Nitrite ◽  
Inducible Nitric Oxide

scholarly journals Effects of hydrocortisone stress-dose therapy in septic shock (part I): influence on hemodynamic stability and plasma nitrite/nitrate levels

Critical Care ◽  
10.1186/cc478 ◽  
1999 ◽  
Vol 3 (Suppl 1) ◽  
pp. P104 ◽  
Author(s):  
D Keh ◽  
S Weber-Carstens ◽  
T Böhnke ◽  
C Schulz ◽  
M Pettersson ◽  
...  
Keyword(s):  
Septic Shock ◽  
Hemodynamic Stability ◽  
Dose Therapy ◽  
Nitrite Nitrate ◽  
Plasma Nitrite ◽  
Stress Dose

scholarly journals Plasma nitrite/nitrate level is inversely correlated with plasma low-density lipoprotein cholesterol level

1997 ◽  
Vol 20 (4) ◽  
pp. 361-365 ◽  
Author(s):  
Seiya Tanaka ◽  
Akira Yashiro ◽  
Masaharu Ikeda ◽  
Akio Kuroiwa ◽  
Yasuhide Nakashima ◽  
...  
Keyword(s):  
Cholesterol Level ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Lipoprotein Cholesterol ◽  
Low Density ◽  
Low Density Lipoprotein Cholesterol ◽  
Nitrate Level ◽  
Nitrite Nitrate ◽  
Plasma Nitrite

Enhancement of the inducible NO synthase activation by retinoic acid is mimicked by RARα agonist in vivo

2002 ◽  
Vol 283 (3) ◽  
pp. E525-E535 ◽  
Author(s):  
Carole Seguin-Devaux ◽  
Yvan Devaux ◽  
Véronique Latger-Cannard ◽  
Sandrine Grosjean ◽  
Cécile Rochette-Egly ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Retinoic Acid Receptor ◽  
Interferon Γ ◽  
Relative Contribution ◽  
All Trans Retinoic Acid ◽  
X Receptors ◽  
Retinoic Acid Receptor Α ◽  
Nitrite Nitrate ◽  
Plasma Nitrite

We have previously shown that all- trans retinoic acid (atRA), the active metabolite of vitamin A, enhances the activation of the inducible nitric oxide synthase (NOS II) pathway, a component of innate immunity, in rats in vivo. We investigated the relative contribution of retinoic acid receptor-α (RARα) and retinoid X receptors (RXRs) to NOS II activation triggered by LPS. Five-day supplementation with 10 mg/kg of either atRA or the RARα selective agonist Ro-40-6055, but not with 10 mg/kg of the pan-RXR agonist Ro-25-7386, enhanced the LPS-induced NOS II mRNA, protein expression in liver, and plasma nitrite/nitrate concentration. Both atRA and the RARα agonist (but not the RXR agonist) increased the number of peripheral T helper lymphocytes and plasma interferon-γ concentration. Synergism between retinoids and LPS on NOS II activation within an organ coincided with synergism on interferon regulatory factor-1 mRNA expression but not with the level of expression of the RARα protein. These results suggest that, in vivo, atRA activates NOS II through RARα and contributes to characterizing the complex effect of retinoids on the host inflammatory/immune response.

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