L-Arginine

The seeds of Glycine max

H-Arg-OH

L-Arginine and its metabolites in kidney and cardiovascular disease.[Pubmed:25161088]

Amino Acids. 2014 Oct;46(10):2271-86.

L-Arginine is a semi essential amino acid synthesised from glutamine, glutamate and proline via the intestinal-renal axis in humans and most mammals. L-Arginine degradation occurs via multiple pathways initiated by arginase, nitric-oxide synthase, Arg: glycine amidinotransferase, and Arg decarboxylase. These pathways produce nitric oxide, polyamines, proline, glutamate, creatine and agmatine with each having enormous biological importance. Several disease are associated to an L-Arginine impaired levels and/or to its metabolites: in particular various L-Arginine metabolites may participate in pathogenesis of kidney and cardiovascular disease. L-Arginine and its metabolites may constitute both a marker of pathology progression both the rationale for manipulating L-Arginine metabolism as a strategy to ameliorate these disease. A large number of studies have been performed in experimental models of kidney disease with sometimes conflicting results, which underlie the complexity of Arg metabolism and our incomplete knowledge of all the mechanisms involved. Moreover several lines of evidence demonstrate the role of L-arg metabolites in cardiovascular disease and that L-arg administration role in reversing endothelial dysfunction, which is the leading cause of cardiovascular diseases, such as hypertension and atherosclerosis. This review will discuss the implication of the mains L-Arginine metabolites and L-Arginine-derived guanidine compounds in kidney and cardiovascular disease considering the more recent literature in the field.

Oral supplementation with a combination of L-citrulline and L-arginine rapidly increases plasma L-arginine concentration and enhances NO bioavailability.[Pubmed:25445598]

Biochem Biophys Res Commun. 2014 Nov 7;454(1):53-7.

BACKGROUND: Chronic supplementation with L-citrulline plus L-Arginine has been shown to exhibit anti-atherosclerotic effects. However, the short-term action of this combination on the nitric oxide (NO)-cGMP pathway remains to be elucidated. The objective of the present study was to investigate the acute effects of a combination of oral L-citrulline and L-Arginine on plasma L-Arginine and NO levels, as well as on blood circulation. METHODS: Rats or New Zealand white rabbits were treated orally with L-citrulline, or L-Arginine, or a combination of each at half dosage. Following supplementation, plasma levels of L-Arginine, NOx, cGMP and changes in blood circulation were determined sequentially. RESULTS: L-Citrulline plus L-Arginine supplementation caused a more rapid increase in plasma L-Arginine levels and marked enhancement of NO bioavailability, including plasma cGMP concentrations, than with dosage with the single amino acids. Blood flow in the central ear artery in rabbits was also significantly increased by L-citrulline plus L-Arginine administration as compared with the control. CONCLUSION: Our data show for the first time that a combination of oral L-citrulline and L-Arginine effectively and rapidly augments NO-dependent responses at the acute stage. This approach may have clinical utility for the regulation of cardiovascular function in humans.

L-Arginine modulates neonatal lymphocyte proliferation through an interleukin-2 independent pathway.[Pubmed:24697328]

Immunology. 2014 Oct;143(2):184-92.

In cases of arginine depletion, lymphocyte proliferation, cytokine production and CD3zeta chain expression are all diminished. In addition to myeloid suppressor cells, polymorphonuclear cells (PMN) also exert T-cell immune suppressive effects through arginase-induced L-Arginine depletion, especially during pregnancy. In this study, we investigated how arginase/L-Arginine modulates neonatal lymphocyte proliferation. Results showed that the neonatal plasma L-Arginine level was lower than in adults (48.1 +/- 11.3 versus 86.5 +/- 14.6 mum; P = 0.003). Neonatal PMN had a greater abundance of arginase I protein than adult PMN. Both transcriptional regulation and post-transcriptional regulation were responsible for the higher arginase I expression of neonatal PMN. Exogenous L-Arginine enhanced neonate lymphocyte proliferation but not that of adult cells. The RNA-binding protein HuR was important but was not the only modulation factor in L-Arginine-regulated neonatal T-cell proliferation. L-Arginine-mediated neonatal lymphocyte proliferation could not be blocked by interleukin-2 receptor blocking antibodies. These results suggest that the altered arginase/L-Arginine cascade may be one of the mechanisms that contribute to altered neonatal immune responses. Exogenous L-Arginine could enhance neonate lymphocyte proliferation through an interleukin-2-independent pathway.

Modulatory effects of l-arginine and soy enriched diet on bone homeostasis abnormalities in streptozotocin-induced diabetic rats.[Pubmed:25617479]

Chem Biol Interact. 2015 Mar 5;229:9-16.

Diabetes mellitus is a complex syndrome which is responsible for numerous complications affecting the whole body. Osteoporosis is regarded as one of the chronic complications of diabetes mellitus that results from reduced bone formation and increased resorption. In this context, we searched for dietary supplements that preserve diabetic bone loss. Parathyroid hormone (PTH) has been suggested as a possible mechanism affecting bone homeostasis in streptozotocin (STZ)-induced diabetic rats. The osteoprotective effects of L-Arginine and soy enriched diet were also investigated. Male Wistar rats were allocated into four groups; normal control, untreated STZ-diabetic rats and STZ-diabetic rats treated with either L-Arginine (10mg/kg/day) or fed soy enriched diet (200 g/kg diet) for 12 weeks. L-Arginine and soy enriched diet normalized serum PTH level and increased serum osteocalcin level; bone osteocalcin, osteoprotegerin and runt-related transcription factor2 mRNA levels compared to diabetic rats. A decrease in serum pyridinoline, C-terminal telopeptides of type I collagen, cathepsin k levels and bone cathepsin k mRNA level was observed in both treated groups. Both treatments increased serum insulin and insulin like growth factor-1 levels and decreased urinary calcium excretion. In conclusion, L-Arginine and soy enriched diet are effective in prevention of osteoporosis associated with diabetes mellitus.

Insulin secretion from pancreatic B cells caused by L-arginine-derived nitrogen oxides.[Pubmed:1371193]

Science. 1992 Feb 7;255(5045):721-3.

L-Arginine causes insulin release from pancreatic B cells. Data from three model systems support the hypothesis that L-Arginine-derived nitrogen oxides (NOs) mediate insulin release stimulated by L-Arginine in the presence of D-glucose and by the hypoglycemic drug tolbutamide. The formation of NO in pancreatic B cells was detected both chemically and by the NO-induced accumulation of guanosine 3',5'-monophosphate. NG-substituted L-Arginine analogs inhibited the release of both insulin and NO. Protein immunoblot and histochemical analysis with antiserum to type I NO synthase suggest that the formation of NO in pancreatic B cells is catalyzed by an NADPH- (reduced form of nicotinamide adenine dinucleotide phosphate), Ca2+/calmodulin-dependent type I NO synthase of about 150 kilodaltons.

Vascular endothelial cells synthesize nitric oxide from L-arginine.[Pubmed:3131684]

Nature. 1988 Jun 16;333(6174):664-6.

Nitric oxide (NO) released by vascular endothelial cells accounts for the relaxation of strips of vascular tissue and for the inhibition of platelet aggregation and platelet adhesion attributed to endothelium-derived relaxing factor. We now demonstrate that NO can be synthesized from L-Arginine by porcine aortic endothelial cells in culture. Nitric oxide was detected by bioassay, chemiluminescence or by mass spectrometry. Release of NO from the endothelial cells induced by bradykinin and the calcium ionophore A23187 was reversibly enhanced by infusions of L-Arginine and L-citrulline, but not D-arginine or other close structural analogues. Mass spectrometry studies using 15N-labelled L-Arginine indicated that this enhancement was due to the formation of NO from the terminal guanidino nitrogen atom(s) of L-Arginine. The strict substrate specificity of this reaction suggests that L-Arginine is the precursor for NO synthesis in vascular endothelial cells.

L-Arginine is the nitrogen donor for synthesis of nitric oxide, a potent vasodilator that is deficient during times of sickle cell crisis.

L-Arginine,74-79-3,(S)-(+)-Arginine,Natural Products,Amino Acids and Derivatives, buy L-Arginine , L-Arginine supplier , purchase L-Arginine , L-Arginine cost , L-Arginine manufacturer , order L-Arginine , high purity L-Arginine