Arginine is a physiological precursor of endothelium-derived nitric oxide.
ATP dose dependently stimulated the formation and release of nitric oxide (NO) from perfused rabbit aorta. L-Canavanine, an inhibitor of various L-arginine-utilizing enzymes, abolished basal and ATP-induced NO formation and release. ATP increased the accumulation of presumably NO-derived NO2- in the medium of primary cultures of bovine aortic endothelial cells. 15NO, 15NO2- and 15NO3- formation was found when L-[guanido-15N2]arginine was added to the culture medium. We conclude that the terminal guanidino nitrogens of L-arginine are the physiological precursors of endothelium-derived NO.
Schmidt
H H
HH
Institut für Pharmakologie, Freie Universität Berlin, F.R.G.
Nau
H
H
Wittfoht
W
W
Gerlach
J
J
Prescher
K E
KE
Klein
M M
MM
Niroomand
F
F
Böhme
E
E
D000818:Animals; D001013:Aorta, Thoracic / Q000378:metabolism; D001120:Arginine / Q000378:metabolism*; D001685:Biological Factors / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000378:metabolism*; D008401:Gas Chromatography-Mass Spectrometry; D066298:In Vitro Techniques; D008163:Luminescent Measurements; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D009590:Nitrogen Radioisotopes; D011817:Rabbits; D013056:Spectrophotometry, Ultraviolet
D001685:Biological Factors; D009590:Nitrogen Radioisotopes; D009569:Nitric Oxide; D001120:Arginine