QuickView for asymmetric dimethylarginine (compound)

N(G),N(G)-Dimethylarginine; C03626; Guanidino-N,N-dimethylarginine; 102783-24-4; CHEBI:17929; NCGC00015343-01; ADMA; N(G)-Dimethylarginine; N(omega),N(omega)-dimethyl-L-arginine; N(G1),N(G1)-Dimethylarginine.
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N(G),N(G)-Dimethylarginine; C03626; Guanidino-N,N-dimethylarginine; 102783-24-4; CHEBI:17929; NCGC00015343-01; ADMA; N(G)-Dimethylarginine; N(omega),N(omega)-dimethyl-L-arginine; N(G1),N(G1)-Dimethylarginine; N(G),N(G)-dimethyl-L-arginine; N(5)-[(dimethylamino)(imino)methyl]-L-ornithine; N,N-dimethylarginine; Dimethyl-L-arginine; L-Ornithine, N5-((dimethylamino)iminomethyl)-; NG,NG-DIMETHYL-L-ARGININE; DA2; N(5)-((Dimethylamino)iminomethyl)-L-ornithine; Lopac-D-4268; 30315-93-6; (2S)-2-amino-5-{[(dimethylamino)(imino)methyl]amino}pentanoic acid
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N(g)-dimethylarginine; N(g),N(g)-dimethylarginine; N(g),N(g)-dimethyl-l-arginine; Dimethyl-l-arginine; ADMA; N(G1),N(G1)-Dimethylarginine; NG,NG-dimethyl-l-arginine; N(5)-[(dimethylamino)(imino)methyl]-L-ornithine; Guanidino-n,n-dimethylarginine; N(5)-((Dimethylamino)iminomethyl)-L-ornithine.
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N(g)-dimethylarginine; N(g),N(g)-dimethylarginine; N(g),N(g)-dimethyl-l-arginine; Dimethyl-l-arginine; ADMA; N(G1),N(G1)-Dimethylarginine; NG,NG-dimethyl-l-arginine; N(5)-[(dimethylamino)(imino)methyl]-L-ornithine; Guanidino-n,n-dimethylarginine; N(5)-((Dimethylamino)iminomethyl)-L-ornithine; Lopac-D-4268; Asymmetric dimethylarginine; N(omega),N(omega)-dimethyl-l-arginine
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Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, is formed by methylation of arginine residues in proteins and released after proteolysis. In this reaction, S-adenosylmethionine is methyldonor and S-adenosylhomocysteine the demethylated product. ADMA and homocysteine are thus biochemically linked. Both plasma ho...
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Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, is formed by methylation of arginine residues in proteins and released after proteolysis. In this reaction, S-adenosylmethionine is methyldonor and S-adenosylhomocysteine the demethylated product. ADMA and homocysteine are thus biochemically linked. Both plasma homocysteine and ADMA concentrations are increased in patients with renal dysfunction, probably as a result of an impairment in their metabolic, but not urinary, clearance. Hyperhomocysteinemia has been associated with an increased risk of cardiovascular disease in end-stage renal disease, especially in patients without malnutrition and inflammation. Also, plasma ADMA levels have been associated with cardiovascular disease in renal failure patients. Both homocysteine and ADMA are thought to mediate their adverse vascular effects by impairing endothelial, nitric oxide-dependent function resulting in decreased vasodilatation, increased smooth muscle cell proliferation, platelet dysfunction and increased monocyte adhesion.
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