Circulation, Vol 83, 1057-1062, Copyright © 1991 by American Heart Association
JP Cooke, NA Andon, XJ Girerd, AT Hirsch and MA Creager
BACKGROUND. Reduced synthesis of endothelium-derived relaxing factor (EDRF)
may explain impaired endothelium-dependent vasodilation in
hypercholesterolemia. Accordingly, we designed studies to determine if
endothelium-dependent relaxation in hypercholesterolemic rabbits may be
restored by supplying L-arginine, the precursor of EDRF. METHODS AND
RESULTS. Normal or hypercholesterolemic rabbits received intravenous L-
arginine (10 mg/kg/min) or vehicle for 70 minutes. Subsequently, animals
were killed, thoracic aortas were harvested, and vascular rings were
studied in vitro. Rings were contracted by norepinephrine and relaxed by
acetylcholine chloride or sodium nitroprusside. Vasorelaxation was
quantified by determining the maximal response (expressed as percent
relaxation of the contraction) and the ED50 (dose of drug inducing 50%
relaxation; expressed as -log M). In vessels from hypercholesterolemic
animals receiving vehicle, there was a fivefold rightward shift in
sensitivity to acetylcholine compared with normal animals (p = 0.05, n = 5
in each group). In vessels from hypercholesterolemic animals, L-arginine
augmented the maximal response to acetylcholine (83 +/- 16% versus 60 +/-
15%, p = 0.04 versus vehicle) and increased the sensitivity to
acetylcholine (ED50 value: 6.7 +/- 0.2 versus 6.2 +/- 0.2, p less than 0.05
versus vehicle). Arginine did not affect maximal and EC50 responses to
acetylcholine in vessels from normal animals. Arginine did not potentiate
endothelium- independent responses in either group. CONCLUSIONS. We
conclude that the endothelium-dependent relaxation is normalized in
hypercholesterolemic rabbit thoracic aorta by in vivo exposure to L-
arginine, the precursor for EDRF.
ARTICLES
Arginine restores cholinergic relaxation of hypercholesterolemic rabbit thoracic aorta
Division of Vascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston.
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L. Cominacini, A. Rigoni, A. F. Pasini, U. Garbin, A. Davoli, M. Campagnola, A. M. Pastorino, V. Lo Cascio, and T. Sawamura The Binding of Oxidized Low Density Lipoprotein (ox-LDL) to ox-LDL Receptor-1 Reduces the Intracellular Concentration of Nitric Oxide in Endothelial Cells through an Increased Production of Superoxide J. Biol. Chem., April 20, 2001; 276(17): 13750 - 13755. [Abstract] [Full Text] [PDF]
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