Kits
ADMA ELISA
Kits
Description
Asymmetric dimethylarginine (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 dimethylarginine
dimethylaminohydrolase (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 Larginine/NO-metabolism
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.
It is formed during proteolysis of methylated proteins and removed
by renal excretion or metabolic degradation by the enzyme dimethylarginine
dimethylaminohydrolase (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 Larginine/NO-metabolism
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.