scholarly journals Effect of renal function on serum nitrogen oxide concentrations

1996 ◽  
Vol 42 (3) ◽  
pp. 440-444 ◽  
Author(s):  
I M Mackenzie ◽  
A Ekangaki ◽  
J D Young ◽  
C S Garrard

Abstract Nitric oxide is too short-lived to measure in vivo, but its production can be estimated by measuring its stable oxidation products, nitrites and nitrates, in serum. Renal elimination of these ions has been demonstrated, but the effect of renal function on their concentrations in serum is currently unknown. We evaluated serum and urine nitrates + nitrites as serum nitrogen oxides (sNOx), nitrogen oxide (NOx) clearance, and creatinine clearance in 71 patients on the Intensive Therapy Unit. The correlation between sNOx and plasma creatinine was strong and highly significant (P <0.001). These results suggest that renal function has a significant effect on sNOx concentrations. Studies in which the sNOx concentration is used as an index of nitric oxide production can therefore be interpreted only if renal function has been taken into account.

2003 ◽  
Vol 31 (11) ◽  
pp. 1337-1346 ◽  
Author(s):  
Jose A. Adams ◽  
James E. Moore, Jr. ◽  
Michael R. Moreno ◽  
Jaqueline Coelho ◽  
Jorge Bassuk ◽  
...  

1995 ◽  
Vol 181 (1) ◽  
pp. 63-70 ◽  
Author(s):  
N K Worrall ◽  
W D Lazenby ◽  
T P Misko ◽  
T S Lin ◽  
C P Rodi ◽  
...  

The role of nitric oxide in the immune response to allogeneic tissue was explored in an in vivo cardiac transplant model in the rat. Nitric oxide production during organ rejection was demonstrated by elevations in systemic serum nitrite/nitrate levels and by electron paramagnetic resonance spectroscopy. Messenger RNA for the inducible nitric oxide synthase enzyme was detected in the rejecting allografted heart, but not in the nonrejecting isografted heart. The enzyme was demonstrated to be biologically active by the in vitro conversion of L-arginine to L-citrulline and was immunohistochemically localized to the infiltrating inflammatory cells. Treatment with aminoguanidine, a preferential inhibitor of the inducible nitric oxide synthase isoform, prevented the increased nitric oxide production in the transplanted organ and significantly attenuated the pathogenesis of acute rejection. Aminoguanidine treatment prolonged graft survival, improved graft contractile function, and significantly reduced the histologic grade of rejection. These results suggest an important role for nitric oxide in mediating the immune response to allogeneic tissue. Inhibition of inducible nitric oxide synthase may provide a novel therapeutic modality in the management of acute transplant rejection and of other immune-mediated processes.


Molecules ◽  
2021 ◽  
Vol 26 (19) ◽  
pp. 5843
Author(s):  
Shaila Mehwish ◽  
Sanjay Varikuti ◽  
Mubarak Ali Khan ◽  
Tariq Khan ◽  
Imdad Ullah Khan ◽  
...  

Natural products from plants contain many interesting biomolecules. Among them, quercetin (Q), gallic acid (GA), and rutin (R) all have well-reported antileishmanial activity; however, their exact mechanisms of action are still not known. The current study is a step forward towards unveil the possible modes of action of these compounds against Leishmania donovani (the causative agent of visceral leishmaniasis). The selected compounds were checked for their mechanisms of action against L. donovani using different biological assays including apoptosis and necrosis evaluation, effects on genetic material (DNA), quantitative testing of nitric oxide production, ultrastructural modification via transmission electron microscopy, and real-time PCR analysis. The results confirmed that these compounds are active against L. donovani, with IC50 values of 84.65 µg/mL, 86 µg/mL, and 98 µg/mL for Q, GA, and R, respectively. These compounds increased nitric oxide production and caused apoptosis and DNA damage, which led to changes in the treated cells’ ultrastructural behavior and finally to the death of L. donovani. These compounds also suppressed essential enzymes like trypanothione reductase and trypanothione synthetase, which are critical for leishmanial survival. The selected compounds have high antileishmanial potentials, and thus in-vivo testing and further screening are highly recommended.


Author(s):  
Yang Guo ◽  
Michael E. Ward ◽  
Stephan Beasjours ◽  
Masataka Mori ◽  
Sabah N.A. Hussain

Stroke ◽  
1995 ◽  
Vol 26 (9) ◽  
pp. 1627-1633 ◽  
Author(s):  
Anish Bhardwaj ◽  
Frances J. Northington ◽  
Raymond C. Koehler ◽  
Theodore Stiefel ◽  
Daniel F. Hanley ◽  
...  

2000 ◽  
Vol 14 (10) ◽  
pp. 1447-1454 ◽  
Author(s):  
Takaaki Akaike ◽  
Shigemoto Fujii ◽  
Atsushi Kato ◽  
Jun Yoshitake ◽  
Yoichi Miyamoto ◽  
...  

2019 ◽  
Vol 7 (4) ◽  
pp. 65
Author(s):  
Leguina-Ruzzi ◽  
Ortiz Diban ◽  
Velarde

Type 2 diabetes affects over 340 million people worldwide. This condition can go unnoticed and undiagnosed for years, leading to a late stage where high glycaemia produces complications such as delayed wound healing. Studies have shown that 12-HHT through BLT2, accelerates keratinocyte migration and wound healing. Additionally, evidence has shown the role of nitric oxide as a pro-regenerative mediator, which is decreased in diabetes. Our main goal was to study the association between the 12-HHT/BLT2 axis and the nitric oxide production in wound healing under different glycaemia conditions. For that purpose, we used in vivo and in vitro models. Our results show that the skin from diabetic mice showed reduced BLT2 and iNOS mRNA, TEER, 12-HHT, nitrites, and tight junction levels, accompanied by higher MMP9 mRNA levels. Furthermore, a positive correlation between BLT2 mRNA and nitrites was observed. In vitro, HaCaT-BLT2 cells showed higher nitric oxide and tight junction levels, and reduced MMP9 mRNA levels, compared to mock-keratinocytes under low and high glucose condition. The wound healing capacity was associated with higher nitric oxide production and was affected by the NOS inhibition. We suggest that the BLT2 expression improves the keratinocyte response to hyperglycaemia, associated with the production of nitric oxide.


2007 ◽  
Vol 293 (3) ◽  
pp. E776-E782 ◽  
Author(s):  
Paolo Tessari ◽  
Anna Coracina ◽  
Lucia Puricelli ◽  
Monica Vettore ◽  
Alessandra Cosma ◽  
...  

Nitric oxide (NO) is a key regulatory molecule with wide vascular, cellular, and metabolic effects. Insulin affects NO synthesis in vitro. No data exist on the acute effect of insulin on NO kinetics in vivo. By employing a precursor-product tracer method in humans, we have directly estimated the acute effect of insulin on intravascular NOx (i.e., the NO oxidation products) fractional (FSR) and absolute (ASR) synthesis rates in vivo. Nine healthy male volunteers were infused iv with l-[15N2-guanidino]arginine ([15N2]arginine) for 6 h. Timed measurements of 15NOx and [15N2]arginine enrichments in whole blood were performed in the first 3 h in the fasting state and then following a 3-h euglycemic-hyperinsulinemic clamp (with plasma insulin raised to ≈1,000 pmol/l). In the last 60 min of each experimental period, at ≈steady-state arginine enrichment, a linear increase of 15NOx enrichment (mean r = 0.9) was detected in both experimental periods. In the fasting state, NOx FSR was 27.4 ± 4.3%/day, whereas ASR was 0.97 ± 0.36 mmol/day, accounting for 0.69 ± 0.27% of arginine flux. Following hyperinsulinemia, both FSR and ASR of NOx increased (FSR by ≈50%, to 42.4 ± 6.7%/day, P < 0.005; ASR by ≈25%, to 1.22 ± 0.41 mmol/day, P = 0.002), despite a ≈20–30% decrease of arginine flux and concentration. The fraction of arginine flux used for NOx synthesis was doubled, to 1.13 ± 0.35% ( P < 0.003). In conclusion, whole body NOx synthesis can be directly measured over a short observation time with stable isotope methods in humans. Insulin acutely stimulates NOx synthesis from arginine.


1992 ◽  
Vol 262 (4) ◽  
pp. C1077-C1082 ◽  
Author(s):  
T. R. Billiar ◽  
R. D. Curran ◽  
B. G. Harbrecht ◽  
J. Stadler ◽  
D. L. Williams ◽  
...  

Hepatocytes are known to synthesize nitric oxide (NO) from L-arginine via an inducible NO synthase. Studies were performed to determine the relationship between hepatocyte NO production and the stimulation of hepatocyte soluble guanylate cyclase. A combination of lipopolysaccharide (LPS), interferon-gamma, tumor necrosis factor, and interleukin-1 stimulates the biosynthesis of large quantities of nitrite and nitrate (NO2- + NO3-). Hepatocyte NO2- + NO3- production was associated with only small increases in intracellular guanosine 3',5'-cyclic monophosphate (cGMP) levels but much greater increases in extracellular cGMP release over an 18-h time period. This cGMP synthesis was dependent on the L-arginine concentration and was inhibited in a reversible manner by NG-monomethyl-L-arginine. The cytokines or LPS added alone induced small increases in nitrogen oxide production and concomitant minor elevations in cGMP release. Atrial natriuretic peptide also stimulated the release of cGMP by hepatocytes which appeared to be independent of the cytokine+LPS-induced cGMP release. The addition of probenecid reduced the cGMP release by 66%, while cell damage was excluded as a cause for the extracellular release. Addition of 3-isobutyl-1-methylxanthine, but not M&B 22948, increased hepatocyte intra- and extracellular cGMP levels after cytokine+LPS stimulation. Induction of nitrogen oxide synthesis by hepatocytes in vivo by injecting rats with killed Corynebacterium parvum resulted in increased cGMP levels in freshly isolated hepatocytes and increased cGMP release by the hepatocytes when placed in culture.(ABSTRACT TRUNCATED AT 250 WORDS)


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