For research use only. Not for therapeutic Use.
L-Arginine is the nitrogen donor for synthesis of nitric oxide, a potent vasodilator that is deficient during times of sickle cell crisis.<br>L-Arginine (0.3 mM, 30 minutes) supplementation do not induce any significant increases in the peak NO concentration at low level of native LDL. However, at native LDL concentrations from 60-130 mg cholesterol/dL, NO concentration is 2 times higher than before L-Arginine treatment in bovine aortic endothelial cells. L-Arginine (0.3 mM, 30 minutes) pretreatment results in a significant increase of NO production in n-LDL–treated cells as well as in oxidized -LDL–treated cells in bovine aortic endothelial cells. L-Arginine (0.3 mM, 30 minutes) does not increase O<sub>2</sub><br>L-Arginine (4 mg/kg/min for 1 hour) treatment decreases superoxide generation by cNOS while increasing NO accumulation in rabbit limb during ischemia/reperfusion. L-Arginine (4 mg/kg/min for 1 hour) prevents microvessel constriction in the reperfused muscle despite reduced but still apparent interstitial edema in rabbit limb. L-Arginine (4 mg/kg/min for 1 hour) treatment results in a significant reduction of muscular reperfusion edema in rabbit limb.
Catalog Number | A001157 |
CAS Number | 1119-34-2 |
Synonyms | NA |
Molecular Formula | C6H14N4O2.HCl |
Purity | ≥95% |
Target | Immunology/Inflammation |
Storage | 3 years -20C powder |