Accumulation of an endogenous inhibitor of nitric oxide synthesis in chronic renal failure

@article{Leone1992AccumulationOA,
  title={Accumulation of an endogenous inhibitor of nitric oxide synthesis in chronic renal failure},
  author={A. M. Leone and Salvador Moncada and Patrick Vallance and Alison L. Calver and Joe Collier},
  journal={The Lancet},
  year={1992},
  volume={339},
  pages={572-575}
}
Total nitric oxide production is low in patients with chronic renal disease.
TLDR
Twenty-four-hour urinary NOX excretion was low in CRD patients compared with controls despite similar dietary NO intake, suggesting that net endogenous NO production is decreased in renal disease.
Arginine, arginine analogs and nitric oxide production in chronic kidney disease
  • C. Baylis
  • Biology
    Nature Clinical Practice Nephrology
  • 2006
TLDR
Because an increase in ADMA has emerged as a major independent risk factor in end-stage renal disease (and probably also in CKD), lowering ADMA concentration is a major therapeutic goal; interventions that enhance the activity of the ADMA-hydrolyzing enzyme DDAH are under investigation.
Nitric oxide in essential and renal hypertension.
TLDR
In dialysis-dependent renal failure, the accumulation of endogenous compounds that inhibit NO synthase could exacerbate renal hypertension by inhibiting vascular and renal tubular NO synthesis and might provoke atherogenesis.
Effect of chronic renal failure on nitric oxide metabolism.
  • N. Vaziri
  • Biology, Medicine
    American journal of kidney diseases : the official journal of the National Kidney Foundation
  • 2001
TLDR
The purpose of this review is to provide a brief overview of the effect of CRF on the bioavailability of NO substrate, L-arginine; the expression of NOS isoforms in the relevant organs; the interaction of NO with reactive oxygen species that are known to be increased in CRF, and the accumulation of uremic inhibitors of N OS.
Nitric oxide in chronic renal failure.
TLDR
Investigation showed an unimpaired availability of NO under baseline conditions but a profound reduction of agonist-induced endothelium-dependent vasodilatation in uremic patients, and suggested only a minor role for cytochrome-P450 2C9-dependent pathways in this context.
Nitric oxide deficiency in chronic kidney disease.
  • C. Baylis
  • Biology
    American journal of physiology. Renal physiology
  • 2008
TLDR
Interventions that can restore NO production by targeting these various pathways are likely to reduce the cardiovascular complications of CKD as well as slowing the rate of progression.
Asymmetrical dimethylarginine, an endogenous nitric oxide synthase inhibitor, in experimental hypertension.
TLDR
ADMA, independently of the renal dimethylargininase content, may play a role in the pathogenesis in Dahl salt-sensitive hypertensive rats but not in SHR, and the results suggest that the systemic production of ADMA is not dependent on renal dim methylargin inase.
Indices of activity of the nitric oxide system in hemodialysis patients.
  • R. Schmidt, J. Domico, C. Baylis
  • Medicine, Biology
    American journal of kidney diseases : the official journal of the National Kidney Foundation
  • 1999
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 25 REFERENCES
Role of endothelium-derived nitric oxide in the regulation of blood pressure.
  • D. Rees, R. Palmer, S. Moncada
  • Biology, Medicine
    Proceedings of the National Academy of Sciences of the United States of America
  • 1989
TLDR
Results indicate that nitric oxide formation from L-arginine by the vascular endothelium plays a role in the regulation of blood pressure and in the hypotensive actions of acetylcholine.
Effects of Amino Acid Infusion on Renal Hemodynamics: Role of Endothelium‐Derived Relaxing Factor
TLDR
It is concluded that Endotheliumderived relaxing factor may participate in the renal hemodynamic response to amino acid infusion and participate in regulation of basal renal hemodynamics.
The involvement of endothelium‐derived relaxing factor in the regulation of renal cortical blood flow in the rat
TLDR
The findings suggest that MeArg and NO2Arg inhibit basal and ACh‐stimulated release of NO in the renal cortical vasculature, indicating that endogenous NO formation may play an important role in the local regulation of renal cortical blood flow.
Glucagon and prostaglandins are mediators of amino acid-induced rise in renal hemodynamics.
An oral protein load or infusion of amino acids induces a rise in renal hemodynamics in normal subjects, but the mechanisms mediating this phenomenon are unknown. We investigated whether glucagon may
Vascular endothelial cells synthesize nitric oxide from L-arginine
TLDR
It is demonstrated that NO can be synthesized from L-arginine by porcine aortic endothelial cells in culture and the strict substrate specificity of this reaction suggests that L- arginine is the precursor for NO synthesis in vascular endothelium cells.
Urinary nitrate excretion in relation to murine macrophage activation. Influence of dietary L-arginine and oral NG-monomethyl-L-arginine.
TLDR
Total body nitrogen oxidation metabolism was measured in vivo by determining the urinary nitrate excretion of mice ingesting a chemically defined nitrite/nitrate-free diet, and it was suggested that L-arginine was synthesized endogenously because there are no other known natural substrates for NOM.
Glucocorticoids inhibit the induction of nitric oxide synthase in macrophages.
Urinary excretion of methylarginine in human disease.
...
1
2
3
...