Article date: February 1989
By: Daryl D. Rees, Richard M.J. Palmer, Harold F. Hodson, Salvador Moncada in Volume 96, Issue 2, pages 418-424
The role of l‐arginine in the basal and stimulated generation of nitric oxide (NO) for endothelium‐dependent relaxation was studied by use of NG‐monomethyl l‐arginine (l‐NMMA), a specific inhibitor of this pathway.
l‐Arginine (10–100 μm), but not d‐arginine (100 μm), induced small but significant endothelium‐dependent relaxations of rings of rabbit aorta. In contrast, l‐NMMA (1–300 μm) produced small, endothelium‐dependent contractions, while its enantiomer NG‐monomethyl‐d‐arginine (d‐NMMA; 100 μ) had no effect.
l‐NMMA (1–300 μm) inhibited endothelium‐dependent relaxations induced by acetylcholine (ACh), the calcium ionophore A23187, substance P or l‐arginine without affecting the endothelium‐independent relaxations induced by glyceryl trinitrate or sodium nitroprusside.
The inhibition of endothelium‐dependent relaxation by l‐NMMA (30 μm) was reversed by l‐arginine (3–300 μm) but not by d‐arginine (300 μm) or a number of close analogues (100 μm).
The release of NO induced by ACh from perfused segments of rabbit aorta was also inhibited by l‐NMMA (3–300 μm), but not by d‐NMMA (100 μm) and this effect of l‐NMMA was reversed by l‐arginine (3–300 μm).
These results support the proposal that l‐arginine is the physiological precursor for the basal and stimulated generation of NO for endothelium‐dependent relaxation.
The role of l‐arginine in the basal and stimulated generation of nitric oxide (NO) for endothelium‐dependent relaxation was studied by use of NG‐monomethyl l‐arginine (l‐NMMA), a specific inhibitor of this pathway.
l‐Arginine (10–100 μm), but not d‐arginine (100 μm), induced small but significant endothelium‐dependent relaxations of rings of rabbit aorta. In contrast, l‐NMMA (1–300 μm) produced small, endothelium‐dependent contractions, while its enantiomer NG‐monomethyl‐d‐arginine (d‐NMMA; 100 μ) had no effect.
l‐NMMA (1–300 μm) inhibited endothelium‐dependent relaxations induced by acetylcholine (ACh), the calcium ionophore A23187, substance P or l‐arginine without affecting the endothelium‐independent relaxations induced by glyceryl trinitrate or sodium nitroprusside.
The inhibition of endothelium‐dependent relaxation by l‐NMMA (30 μm) was reversed by l‐arginine (3–300 μm) but not by d‐arginine (300 μm) or a number of close analogues (100 μm).
The release of NO induced by ACh from perfused segments of rabbit aorta was also inhibited by l‐NMMA (3–300 μm), but not by d‐NMMA (100 μm) and this effect of l‐NMMA was reversed by l‐arginine (3–300 μm).
These results support the proposal that l‐arginine is the physiological precursor for the basal and stimulated generation of NO for endothelium‐dependent relaxation.
DOI: 10.1111/j.1476-5381.1989.tb11833.x
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