N-Methylarginine is an inhibitor of nitric oxide synthase.[1][2] Chemically, it is a methyl derivative of the amino acid arginine. It is used as a biochemical tool in the study of physiological role of nitric oxide.
 (S)-Methylarginine
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| Other names
2-Amino-5-[(N’-methylcarbamimidoyl)amino]pentanoic acid; N-Monomethylarginine; omega-N-Methylarginine; Tilarginine; Targinine
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| Identifiers | |
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3D model (JSmol)
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| 2262067 (R) | |
| ChEBI | |
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| KEGG | |
| MeSH | omega-N-Methylarginine |
PubChem CID
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| UNII | |
CompTox Dashboard (EPA)
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| Properties | |
| C7H16N4O2 | |
| Molar mass | 188.231 g·mol−1 |
| log P | −0.63 |
| Acidity (pKa) | 2.512 |
| Basicity (pKb) | 11.488 |
| Related compounds | |
Related alkanoic acids
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Related compounds
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Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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The inhibiting effect of N-methylarginine on vasodilation is lower in hypertensive patients than in normal subjects, indicating endothelial dysfunction.[3] The inhibiting effect of N-methylarginine on vasodilation declines progressively with age, but has been restored with vitamin C in the oldest subjects.[3]
See also
editReferences
edit- ^ Toutouzas, K.; Riga, M.; Stefanadi, E.; Stefanadis, C. (2008). "Asymmetric dimethylarginine (ADMA) and other endogenous nitric oxide synthase (NOS) inhibitors as an important cause of vascular insulin resistance". Hormone and Metabolic Research. 40 (9): 655–659. doi:10.1055/s-0028-1083814. PMID 18792879. S2CID 260167230.
- ^ Stefanovic-Racic M, Meyers K, Meschter C, Coffey JW, Hoffman RA, Evans CH (1994). "N-monomethyl arginine, an inhibitor of nitric oxide synthase, suppresses the development of adjuvant arthritis in rats". Arthritis & Rheumatology. 37 (7): 1062–1069. doi:10.1002/art.1780370712. PMID 7517676.
- ^ a b Taddei S, Virdis A, Ghiadoni L, Salvetti G, Bernini G, Magagna A, Salvetti A (2012). "Age-related reduction of NO availability and oxidative stress in human". Hypertension. 38 (2): 274–279. CiteSeerX 10.1.1.576.255. doi:10.1161/01.hyp.38.2.274. PMID 11509489.
Up to the age of 60 years, despite the evident decline in endothelium-dependent vasodilation, vitamin C did not modify the response to acetylcholine. In contrast, in the oldest individuals (age >60 years) characterized by a profound alteration in NO availability, vitamin C not only enhanced the response to the endothelial agonist but also restored the inhibiting effect of L-NMMA on vasodilation to acetylcholine.