ADMA Xpress ELISA

Asymmetric dimethyl arginine (ADMA) is an endogenous inhibitor of NOsynthase.
It is formed during proteolysis of methylated proteins and removed by
renal excretion or metabolic degradation by the enzyme
dimethylargininedimethylaminohydrolase (DDAH). Several cell types, including
human endothelial and tubular cells are capable of synthesizing and
metabolizing ADMA. Elevated ADMA concentrations in the blood are found in
numerous diseases associated with endothelial dysfunction. For example,
elevated ADMA levels in blood of dialysis patients correlate significantly with the
degree of arteriosclerosis and cardiovascular risk. Furthermore, elevated ADMA
levels are found in patients with hypercholesterolemia, hypertension,
arteriosclerosis, chronic renal failure and chronic heart failure, and are associated
with restrictions in endothelial vasodilatation.
During the last years, the important clinical relevance of the regulation of
vascular tone and structure by nitric oxide (NO) has been shown. Moreover,
there were reports that human endothelial cells produce ADMA as well as nitric
oxide, which points to an endogenous endothelial NO-regulation by ADMA.
Therefore it was assumed that hypertension, arteriosclerosis and immunological
dysfunction in patients with chronic renal failure are connected to a dysfunction
of the L-arginine/NO-metabolism and to ADMA accumulation. The reasons for
the deregulation of the L-arginine/NO-metabolism could only partially be
elucidated. Certainly, there are multiple factors involved in the L-arginine/NOmetabolism
regulation, as for example elevation of free superoxide radicals (O2
-
),
ADMA accumulation and reduced NO-synthase activity.
Prospective clinical studies of the last years demonstrate the increased
importance of ADMA as a novel cardiovascular risk factor.