L-Arginine HCl (L-Arg)

L-Arginine HCl (L-Arg) supplementation (0.3 mM, 30 minutes) does 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 treatment in bovine aortic endothelial cells. This compound results in a significant increase of NO production in n-LDL–treated cells as well as in oxidized -LDL–treated cells in the same cell type. It does not increase O₂^- concentration at low nativeLDL concentrations but reduces O₂^- production by 50% when incubated with n-LDL at concentrations >40 mg cholesterol/dL. Furthermore, it completely abolishes O₂^- production at every oxidized LDL dosage in bovine aortic endothelial cells. [1]

L-Arginine HCl (L-Arg) (4 mg/kg/min for 1 hour) treatment decreases superoxide generation by cNOS while increasing NO accumulation in rabbit limb during ischemia/reperfusion. This compound prevents microvessel constriction in the reperfused muscle despite reduced but still apparent interstitial edema in rabbit limb, and results in a significant reduction of muscular reperfusion edema in rabbit limb. [2] Its supplementation (0.1 g/kg, oral) significantly reduces pulmonary artery systolic pressure by a mean of 15.2% after 5 days of therapy in patients with sickle cell disease. Both L-Arginine and ornithine concentrations increased significantly after 5 days of oral supplementation in patients with sickle cell disease. [3] It is associated with a decrease in cardiac index while stroke index is maintained in patients with severe sepsis. Resolution of shock at 72 hours is achieved by 40% and 24% of the patients in the L-Arginine and placebo cohorts, respectively. [4] This compound (450 mg/kg during a 15-minute period) amplifies and sustains the hyperemia (38%) and increases absolute brain blood flow after eNOS upregulation by chronic simvastatin treatment (2 mg/kg subcutaneously, daily for 14 days) in SV-129 mice. [5]