L-arginine is the physiological precursor for the formation of nitric oxide in endothelium-dependent relaxation.
The formation of nitric oxide (NO) from L-arginine by vascular endothelial cells and its relationship to endothelium-dependent relaxation of vascular rings was studied. The release of NO, measured by bioassay or chemiluminescence, from porcine aortic endothelial cells stimulated with bradykinin was enhanced by infusions of L-, but not D-arginine. The release of 15NO, determined by high resolution mass spectrometry, from L-guanidino 15N (99%) arginine was also observed, indicating that NO is formed from the terminal guanidino nitrogen atom(s) of L-arginine. L-NG-monomethyl arginine (L-NMMA), but not D-NMMA, inhibited both the generation of NO by endothelial cells in culture and the endothelium-dependent relaxation of rabbit aortic rings. Both these effects were reversed by L-arginine. These data indicate that L-arginine is the physiological precursor for the formation of NO which mediates endothelium-dependent relaxation.
Palmer
R M
RM
Wellcome Research Laboratories, Beckenham, Kent, U.K.
Rees
D D
DD
Ashton
D S
DS
Moncada
S
S
D000818:Animals; D001120:Arginine / Q000378:metabolism*; D001681:Biological Assay; D001920:Bradykinin / Q000494:pharmacology; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism*; D007536:Isomerism; D008163:Luminescent Measurements; D009569:Nitric Oxide / Q000378:metabolism*; D013552:Swine; D014664:Vasodilation
D009569:Nitric Oxide; D001120:Arginine; D001920:Bradykinin