ADMA metabolism and clearance

Teerlink, Tom

doi:10.1177/1358836x0501000111

Cited by 135 publications

(102 citation statements)

References 84 publications

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“…There was no independent correlation between creatinine clearance (␤ϭ0.17; Pϭ0.20), eGFR (␤ϭ0.15; Pϭ0. 24), and levels of CRP (␤ϭ0.14; Pϭ0.28) and isoF2␣ (␤ϭ0.17; Pϭ0.18) and ADMA in our cohort.…”

Section: Factors Influencing Adma Levelsmentioning

confidence: 68%

“…19,24 We, therefore, explored the relationship between creatinine clearance/eGFR and ADMA. Interestingly, we found no correlation between these indirect estimates of renal function and ADMA level in our cohort of healthy subjects.…”

Section: Study Limitationsmentioning

confidence: 99%

“…A potential explanation for this may be that, in subjects with normal renal function, clearance of plasma ADMA occurs in part by urinary excretion, with a substantial proportion of ADMA degraded by the intracellular enzyme dimethylarginine dimethylaminohydrolase after uptake from the circulation. 14,19,24 However, creatinine clearance and eGFR are both indirect estimates of renal function. 16,17 Assessing renal function using more sensitive/accurate techniques and its association with circulating ADMA levels would be worthwhile.…”

Section: Study Limitationsmentioning

confidence: 99%

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Asymmetric Dimethylarginine and Reduced Nitric Oxide Bioavailability in Young Black African Men

et al. 2007

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Abstract-Black Africans have a higher incidence of cardiovascular disease than white Europeans. We explored potential mechanisms of this excess risk by assessing endothelium function, inflammatory status (C-reactive protein), oxidative stress (isoprostane-F2␣), and plasma asymmetrical dimethyl arginine (ADMA; an endogenous competitive inhibitor of NO synthase) in each ethnic group. 1 This in part may be explained by an increased prevalence and severity in blacks of some risk factors for atherosclerosis. In particular, in black subjects, essential hypertension has a higher prevalence, earlier onset, and is associated with more severe end-organ damage, including left ventricular hypertrophy, renal failure, and stroke. 1 However, conventional risk factors for cardiovascular disease do not account for all of this increased risk. A recent study demonstrated that black ethnicity is a strong and independent risk factor for the development of peripheral arterial disease, which was not explained by higher levels of diabetes, hypertension, or body mass index. 2 The mechanisms underlying this ethnic predisposition to cardiovascular dysregulation remain unresolved.A number of studies have demonstrated that black subjects have endothelial dysfunction, 3-5 a key step in the initiation/ progression of atherosclerotic vascular disease. A hallmark of endothelial cell dysfunction is a reduction in the bioavailability of the antiatherosclerotic signaling molecule NO. 6 Longitudinal studies have demonstrated that a reduction in NO bioavailability is a predictor of accelerated atherosclerosis. 7,8 NO is generated by a family of NO synthases from L-arginine in a reaction that requires oxygen, reduced nicotinamideadenine dinucleotide phosphate, and essential cofactors, including tetrahydrobiopterin. NO bioavailability is principally determined by a reduction in its biosynthesis and/or inactivation by reactive oxygen species. Asymmetric dimethylargi-

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Section: Factors Influencing Adma Levelsmentioning

confidence: 68%

Section: Study Limitationsmentioning

confidence: 99%

Section: Study Limitationsmentioning

confidence: 99%

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Asymmetric Dimethylarginine and Reduced Nitric Oxide Bioavailability in Young Black African Men

et al. 2007

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“…The enzyme DDAH specifically hydrolyzes these asymmetrically methylated arginine residues to citrulline and methylamines [34,35]. Several groups have demonstrated that modulating DDAH activity can have a profound effect on endothelial NO production [7,36,37].…”

Section: Discussionmentioning

confidence: 99%

Dimethylarginine Dimethylaminohydrolase 2 Gene Polymorphism and Its Association with Asymmetrical Dimethyl Arginine in Hemodialyzed Patients

Yusuf¹,

Thaha²,

Yogiarto³

et al. 2013

OJNeph

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Introduction: Patients with CKD have elevated plasma levels of Asymmetrical Dimethyl Arginine (ADMA), impaired EDRF/NO responses in isolated resistance vessels, and a marked increase in the frequency of cardiovascular events that are predicated by plasma levels of ADMA. ADMA is considered as a risk factor for endothelial dysfunction, progression of chronic kidney disease and a marked increase in the frequency of cardiovascular events that are predicated by plasma levels of ADMA. Elevated ADMA in CKD have been related to a combination of a reduced renal ADMA excretion and a reduced catabolism of ADMA by dimethylarginine dimethylaminohydrolase (DDAH). The current study was undertaken to determine whether there is a correlation between ADMA and SNPs at −449 DDAH 2. Subjects and Methods: It was a cross sectional analytic study, 56 hemodialysis patients and 30 healthy individuals were enrolled. Based on its etiology, HD patients group was further divided in to hypertension (HT) subgroup and non-HT subgroup. Genotyping of the polymorphisms was performed using PCR-based SNP detection methods based on 5'-exonuclease activity assays for rs805305. Results: Heterozygotes were observed as the most abundant genotypes in both groups, followed by GG genotype in the HD patients (30%) and CC (27%) healthy individuals. Among the HT subgroup, the mean plasma levels of ADMA were sequentially higher from genotypes CC, G/C and GG (p = 0.037). Further multiple comparisons between groups using post hoc test showed results that genotype GG and CC were different at 0.05 level of significance. These findings were not found among non HT subgroup. Conclusion: Genetic variation in the DDAH 2 genes is significantly associated with serum ADMA levels in hypertensive HD patients. We observed that carriage of a G at position −449 in the promoter region of the DDAH 2 gene is associated with higher ADMA levels.

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“…The systemic clearance of ADMA occurs upon catalytic hydrolysis by the dimethylarginine dimethylaminohydrolase (DDAH) to L-citrulline and dimethylamine (DMA), membrane transport by SLC7 family members, and urinary excretion of ADMA as well as DMA [194,195]. A correlation between ADMA plasma levels and the severity of disease has been suggested as an analytical reference for disease risk factors [196].…”

Section: Asymmetric Dimethylarginine (Adma)-adma Is a Biogenic Analogmentioning

confidence: 99%

Bioanalytical profile of the l-arginine/nitric oxide pathway and its evaluation by capillary electrophoresis

Boudko

2007

Journal of Chromatography B

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This review briefly summarizes recent progress in fundamental understanding and analytical profiling of the L-arginine/nitric oxide (NO) pathway. It focuses on key analytical references of NO actions and on the experimental acquisition of these references in vivo, with capillary electrophoresis (CE) and high-performance capillary electrophoresis (HPCE) comprising one of the most flexible and technologically promising analytical platform for comprehensive high-resolution profiling of NO-related metabolites. Second aim of this review is to express demands and bridge efforts of experimental biologists, medical professionals and chemical analysis-oriented scientists who strive to understand evolution and physiological roles of NO and to develop analytical methods for use in biology and medicine.

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ADMA metabolism and clearance

Cited by 135 publications

References 84 publications

Asymmetric Dimethylarginine and Reduced Nitric Oxide Bioavailability in Young Black African Men

Asymmetric Dimethylarginine and Reduced Nitric Oxide Bioavailability in Young Black African Men

Dimethylarginine Dimethylaminohydrolase 2 Gene Polymorphism and Its Association with Asymmetrical Dimethyl Arginine in Hemodialyzed Patients

Bioanalytical profile of the l-arginine/nitric oxide pathway and its evaluation by capillary electrophoresis

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