Key result
Pretreatment with 5 mM L-arginine had no effect on the impaired relaxation response to acetylcholine in atherosclerotic rabbit aortae in vitro.
Why the study?
Does L-arginine improve relaxation to acetylcholine in aortae from cholesterol-fed rabbits?
Does L-arginine improve relaxation to acetylcholine in aortae from cholesterol-fed rabbits?
L-arginine supplementation does not restore endothelium-dependent relaxation in atherosclerotic rabbit aortae, suggesting L-arginine deficiency is not the primary cause of this dysfunction.
Answers are grounded in this paper and cite their sources.
L-arginine does not restore endothelial relaxation in this model; leaves open whether substrate deficiency drives human atherosclerosis.
Bioassay studies suggest that impaired endothelium-dependent relaxation in atherosclerotic arteries is due to a reduced release of biologically active endothelium-derived relaxing factor (EDRF). We tested the hypothesis that endothelial dysfunction is caused by deficiency of the EDRF precursor L-arginine. Aortae from normal and cholesterol-fed (1%, 4 months) rabbits were excised and incubated for 1 h with 5 mM L-arginine. Pretreatment with L-arginine had no effect on the relaxation to acetylcholine in normal vessels and was without effect on the impaired response of atherosclerotic arteries to acetylcholine. This finding suggests that L-arginine deficiency is unlikely the underlying cause of impaired endothelium-dependent relaxation in the aorta of cholesterol-fed rabbits.
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Mügge et al. (2008) studied Atherosclerosis. L-arginine vs. Normal vessels / baseline response was evaluated on Relaxation to acetylcholine. Pretreatment with 5 mM L-arginine had no effect on the impaired relaxation response to acetylcholine in atherosclerotic rabbit aortae in vitro.
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