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Discussion:
L-Arginine
Arginine is a conditionally essential amino acid and the principal
substrate for the family of NOS enzymes that catalyze NO
biosynthesis. It is synthesized in the body from the amino acid
citrulline and can also be obtained from dietary protein. Oral
L-arginine supplementation can affect vasodilation, decrease platelet
aggregation, and reduce endothelial monocyte adhesion.2-4 The effect
of L-arginine and its underlying mechanism can vary according
to arginine plasma concentration range, administration route, and
vascular functionality.*2
Vascular endothelial dysfunction is a hallmark of increased
cardiometabolic risk and results from impairment to the synthesis or
bioavailability of NO. In a randomized, double-blind trial comparing
the effects of oral L-arginine (4.5 g/d) with placebo and assessing
postprandial endothelial function, researchers concluded that
L-arginine plays a role in alleviating endothelial dysfunction when
baseline arginine is low.5
However, orally administered L-arginine is
hampered by extensive metabolic processes that impair its ability
to reach the circulatory plasma and be available as a substrate for
NOS. Another contributing factor to arginine not being available
in circulatory plasma as a substrate is the accumulation of a
naturally occurring byproduct of metabolism, known as asymmetric
dimethylarginine (ADMA), which impairs NO formation as it competes
with endogenous L-arginine for NOS binding.6
Further research
is needed to elicit the contributive effect of lower dosages of oral
L-arginine.*
Nitric oxide (NO) is produced cellularly from the amino acid arginine
through the enzymatic action of nitric oxide synthase (NOS) and
has critical roles in regulating the function of organs and systems
throughout the body. Production of NO by vascular endothelium is vital
to blood flow regulation, and inadequate production can adversely
affect blood flow, vascular tone, delivery of nutrients and oxygen, and
other vascular functions.*
