ライフサイエンスコーパス: ADMA

1 ADMA accumulates in various disease states, including re

2 ADMA also has been proposed to be regulated through an a

3 ADMA and homocysteine are biomarkers for and may be medi

4 ADMA is generated by the catabolism of proteins methylat

5 ADMA levels are controlled by dimethylarginine dimethyla

6 ADMA remained the only independent predictor of mortalit

7 ADMA treatment also exacerbated brain microvascular path

8 ADMA treatment induced the brain nitrosative stress and

9 ADMA treatment resulted in elevated ADMA levels in the b

10 ADMA was low in children with SM relative to controls.

11 ADMA, SDMA and their combined sum, which we termed a dim

12 ADMA-induced remodeling of actin cytoskeleton and interc

13 lial dysfunction: implications for the COX-2/ADMA axis.

14 In the absence of BH 4, ADMA dose-dependently increased NOS-derived (*)O 2 (-) g

15 Importantly, cross-talk between IL-4, ADMA, and mitochondrial dysfunction could explain how ob

16 With AF, ADMA (p < 0.01) and sCD40L (p < 0.001) levels increased

17 Age, ADMA concentration, and T2DM, but not insulin resistance

18 arkers of endothelial function (NO(2)(-) and ADMA).

19 g competitive interaction between FGF-23 and ADMA in the risk of renal events (P<0.01 in adjusted ana

20 Both intact FGF-23 and ADMA predicted the incidence rate of renal events in una

21 R remained inversely associated with age and ADMA, whereas ASR was inversely associated with age and

22 2) and increased markers of inflammation and ADMA.

23 Plasma nitrotyrosine and ADMA levels were similar in OSA and control children; ho

24 Both L-NMMA and ADMA are eliminated largely through active metabolism by

25 was associated with a 48% reduction in l-Arg/ADMA and was partially restored with l-Arg supplementati

26 In contrast, l-Arg/ADMA was unchanged in the DDAH-2-silenced cells, and l-A

27 ncentration of asymmetric dimethyl arginine (ADMA) relative to L-arginine, which can lead to greater

28 o form asymmetrically dimethylated arginine (ADMA), while type 2 enzymes form symmetrically dimethyla

29 etric N(omega),N(omega)-dimethyl-l-arginine (ADMA) is an endogenously produced inhibitor of human nit

30 etric N(omega),N(omega)-dimethyl-l-arginine (ADMA).

31 nt in eNOS activity and increased L-arginine/ADMA ratio and DDAH1 expression.

32 In addition, these lower L-arginine/ADMA ratios are associated with reduced lung function an

33 Also in this phenotype, a reduced L-arginine/ADMA was associated with less IgE, increased respiratory

34 The log of plasma L-arginine/ADMA was inversely correlated with BMI in the late- (r =

35 ship was lost after adjusting for L-arginine/ADMA.

36 Arginine:ADMA ratios, but not arginine, were significantly and in

37 Nevertheless, arginine and arginine:ADMA ratios were very low in SM.

38 e bioavailability (reflected by low arginine:ADMA ratios) is therefore comparably low in SM in childr

39 y on amino acids and the myocardial arginine:ADMA ratio and its relation to myocardial glucose metabo

40 The myocardial arginine:ADMA ratio increased during surgery and was significantl

41 ncreasing the plasma and myocardial arginine:ADMA ratio.

42 y augment the myocardial and plasma arginine:ADMA ratio and availability of amino acids.

43 reoperative to postoperative plasma arginine:ADMA ratio correlated with the change in myocardial gluc

44 With treatment, arginine and the arginine:ADMA ratio normalized, but SDMA did not.

45 of a dominant-negative Akt1 also attenuated ADMA-mediated eNOS mitochondrial translocation.

46 ose, duration of statin therapy and baseline ADMA concentrations as potential variables on the WMD be

47 erential metabolites were identified between ADMA and serum-starved cells.

48 1 active site enables PRMT1 to generate both ADMA and SDMA.

49 NOx FSR inversely correlated with both ADMA and SDMA.

50 al) cells were treated with IL-4 followed by ADMA and investigated for oxo-nitrative stress and resul

51 ithelial cells treated with IL-4 followed by ADMA showed exaggerated oxo-nitrative stress and potent

52 nal level, and most of them were restored by ADMA.

53 dimethylaminohydrolase 2, which catabolizes ADMA.

54 [ADMA]) and l-arginine uptake into the cell (ADMA and symmetrical DMA [SDMA]).

55 assess the effect of statins on circulating ADMA levels.

56 Thus, circulating ADMA may be an imprecise marker of renal methylarginine

57 associated with >/=1 of baseline citrulline, ADMA, SDMA, and MMA levels.

58 In contrast, ADMA was significantly related to the arterial stiffness

59 This study supports a role for the DDAH1/ADMA axis on the effect of inflammation and oxidative st

60 tabolize ADMA in vivo resulting in decreased ADMA levels and improved endothelial NO production.

61 thylaminohydrolase, the enzyme that degrades ADMA.

62 Asymmetric dimethylarginine (ADMA) and homocysteine are mechanistically interrelated

63 Asymmetric dimethylarginine (ADMA) and monomethyl arginine (L-NMMA) are endogenously

64 ethylarginines, asymmetric dimethylarginine (ADMA) and N (G)-monomethyl- l-arginine (L-NMMA) regulate

65 ethylarginines, asymmetric dimethylarginine (ADMA) and N(G)-monomethyl-l-arginine, in tumor-bearing m

66 MAs), including asymmetric dimethylarginine (ADMA) and NG-methyl-L-arginine (L-NMMA), are released in

67 infusion and on asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA) concentratio

68 arginine (MMA), asymmetric dimethylarginine (ADMA) and symmetric dimethylarginine (SDMA).

69 23 (FGF-23) and asymmetric dimethylarginine (ADMA) are associated with progression of CKD.

70 vated levels of asymmetric dimethylarginine (ADMA) correlate with risk factors for cardiovascular dis

71 a reduction in asymmetric dimethylarginine (ADMA) enhances endothelial regeneration.

72 on profile, and asymmetric dimethylarginine (ADMA) in patients undergoing HD.

73 monstrated that asymmetric dimethylarginine (ADMA) induces the translocation of endothelial nitric-ox

74 Asymmetric dimethylarginine (ADMA) is an endogenous inhibitor of NO synthesis, and el

75 Asymmetric dimethylarginine (ADMA) is an endogenous metabolite.

76 of NO synthesis asymmetric dimethylarginine (ADMA) is increased.

77 erapy on plasma asymmetric dimethylarginine (ADMA) levels has not been conclusively studied.

78 Asymmetric dimethylarginine (ADMA) plays a crucial role in endothelial function and m

79 thase inhibitor asymmetric dimethylarginine (ADMA) were measured with liquid chromatography coupled w

80 s NOS inhibitor asymmetric dimethylarginine (ADMA), a cardiotoxic hormone whose effects can be preven

81 bolic enzyme of asymmetric dimethylarginine (ADMA), a major endogenous nitric-oxide synthase inhibito

82 Asymmetric dimethylarginine (ADMA), an endogenous inhibitor and uncoupler of nitric o

83 Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase,

84 ncentrations of asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric-oxide (NO) synt

85 Both asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO production, and end

86 lasma levels of asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, an

87 eased levels of asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, ar

88 Asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, un

89 pathobiology is asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor.

90 pathobiology is asymmetric dimethylarginine (ADMA), an endogenous NO synthase inhibitor.

91 with arginine, asymmetric dimethylarginine (ADMA), and hemolysis.

92 le CD40 ligand, asymmetric dimethylarginine (ADMA), and nitrotyrosine levels, as well as 2 iterations

93 hylarginine and asymmetric dimethylarginine (ADMA), but not symmetric dimethylarginine (SDMA).

94 eine (tHcy) and asymmetric dimethylarginine (ADMA), correlate with decreased levels of endothelium-de

95 ine, ornithine, asymmetric dimethylarginine (ADMA), symmetric dimethylarginine (SDMA), and N-monometh

96 Asymmetric dimethylarginine (ADMA), which inhibits NO synthase, is inactivated by N(G

97 thase inhibitor asymmetric dimethylarginine (ADMA).

98 (NOS) inhibitor asymmetric dimethylarginine (ADMA).

99 e and increased asymmetric dimethylarginine (ADMA).

100 PRMT, producing asymmetric dimethylarginine (ADMA).

101 igher levels of asymmetric dimethylarginine (ADMA; P<0.0001), symmetric dimethylarginine (P<0.0001),

102 Asymmetric-dimethylarginine (ADMA) limits NO production by inhibiting NO synthase and

103 se inhibitors asymmetrical dimethylarginine (ADMA) and monomethyl-l-arginine.

104 Plasma asymmetrical dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthas

105 Asymmetrical dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide synthes

106 thase inhibitor asymmetric dimethylarginine [ADMA, via inhibition of dimethylarginine dimethylaminohy

107 al dysfunction (asymmetric dimethylarginine [ADMA]), and platelet-derived inflammation (soluble CD40

108 Asymmetric and symmetric dimethylarginines (ADMA and SDMA) impair nitric oxide bioavailability and h

109 asymmetric and symmetric dimethylarginines (ADMA and SDMA) predict and potentially contribute to end

110 ing nitric oxide synthase (asymmetrical DMA [ADMA]) and l-arginine uptake into the cell (ADMA and sym

111 , and that the pre-existence of the dominant ADMA mark can block the occurrence of SDMA and MMA marks

112 Elevated ADMA and diminished global arginine bioavailability rati

113 ADMA treatment resulted in elevated ADMA levels in the blood and brain of Tg-SwDI mice.

114 To date, it remains unclear whether elevated ADMA levels are merely associated with cardiovascular ri

115 CS patients with elevated ADMA levels were 3.5-fold (95% confidence interval, 1.4

116 unclear which is responsible for endothelial ADMA metabolism and NO regulation.

117 investigate the significance of endothelial ADMA in cardiovascular homeostasis.

118 were treated with a daily dose of exogenous ADMA.

119 ficantly higher in the presence of exogenous ADMA.

120 0.616 for homocysteine and r(2) = 0.595 for ADMA).

121 ct of glutamylcysteine on DDAH activity (for ADMA) and/or cationic amino acid transport requires furt

122 and remained significant after adjusting for ADMA.

123 .9 microM and 1.1 microM were determined for ADMA and L-NMMA, respectively.

124 methyltransferases, which are essential for ADMA formation.

125 iable analysis substituting homocysteine for ADMA demonstrated comparable relationships with arterial

126 Vmax values of 356 and 154 nmols/mg/min for ADMA and L-NMMA, respectively.

127 Hazard ratios for ADMA and MMA at 2 months were 3.33 (95% confidence inter

128 hydrolase (DDAH) enzymes are responsible for ADMA breakdown.

129 ted peptide and provide sufficient space for ADMA formation.

130 Free ADMA is actively metabolized by the intracellular enzyme

131 is enzymatic activity was selective for free ADMA and L-NMMA and was incapable of hydrolyzing peptide

132 AGXT2 also protected endothelial cells from ADMA-mediated inhibition of NO production.

133 overexpression of human AGXT2 protects from ADMA-induced inhibition in nitric oxide (NO) production.

134 Furthermore, ADMA enhanced Akt1 nitration and increased its activity.

135 of arginine, arginase, cell-free hemoglobin, ADMA, symmetric-dimethylarginine (SDMA), histidine-rich

136 ovel understanding of how obesity, with high ADMA levels, and asthma, with high IL-4 levels, might po

137 3) were independently associated with higher ADMA concentrations; and b) age (P = 0.001), absence of

138 However, ADMA levels did not correlate with negative coronary rem

139 However, ADMA treatment had no such effects on wild type mice.

140 es (DDAHs), cytosolic enzymes that hydrolyze ADMA to citrulline and dimethylamine.

141 matics and healthy controls to evaluate: (i) ADMA-mediated NOS uncoupling reduces epithelial producti

142 Thus, our study identifies ADMA as a biomarker and mechanistic bridge between renal

143 stiffness, was associated with a decrease in ADMA.

144 ion vector produced significant decreases in ADMA levels in plasma and liver.

145 in arginine and citrulline and increases in ADMA were observed at 1 and 2 months (all p < 0.05).

146 ated with the interindividual variability in ADMA, l-arginine, and SDMA.

147 Concentrations of amino acids including ADMA were analyzed in myocardial tissue and plasma sampl

148 PPIs increase ADMA because they bind to and inhibit dimethylarginine d

149 ntracellular ADMA accumulation and increased ADMA-induced mitotoxicity.

150 diated by blocking renal COX-2 and increased ADMA.

151 Consequently, increased ADMA is associated with cardiovascular disease.

152 expression necessarily results in increased ADMA synthesis and demonstrate that enzymatic activity c

153 r portal pressures associated with increased ADMA, which may result from both decreased breakdown (de

154 Increasing ADMA reduces NO formation and increases oxidative and ni

155 ey asthma-associated cytokine, can influence ADMA-related effects on lungs.

156 endothelial nitric oxide synthase inhibitor ADMA as a biomarker and mechanistic bridge between renal

157 circulating nitric oxide synthase inhibitor ADMA was found in children with OSA, soluble CD40 ligand

158 y producer of the competitive NOS inhibitor, ADMA.

159 reated with either PBS or the NOS inhibitors ADMA or N(omega)-nitro-L-arginine methyl ester (L-NAME;

160 was associated with increased intracellular ADMA accumulation and increased ADMA-induced mitotoxicit

161 We conclude that IL-4 promotes intracellular ADMA accumulation, leading to mitochondrial loss through

162 thelial cells, indicating that intracellular ADMA is a critical determinant of endothelial cell respo

163 t mechanisms, the former of which is largely ADMA-dependent and the latter ADMA-independent.

164 ich is largely ADMA-dependent and the latter ADMA-independent.

165 ely to die in 30 days than patients with low ADMA levels.

166 MMF, was associated with significantly lower ADMA levels (0.65+/-0.12 vs. 0.77+/-0.10 micromol/L; P<0

167 s (rather than MMF) is associated with lower ADMA levels and reduced risk of accelerated CAV.

168 aque formation in ApoE(-/-) mice by lowering ADMA.

169 We hypothesized that lowering ADMA concentrations by dimethylarginine dimethylaminohyd

170 uman AGXT2 is able to effectively metabolize ADMA in vivo resulting in decreased ADMA levels and impr

171 nthase inhibitor, asymmetric methylarginine (ADMA) is associated with vascular dysfunction and endoth

172 ith a maximal increase of 151% at 100 microM ADMA.

173 observed in isolated vessels where 5 microm ADMA inhibited vascular relaxation to acetylcholine.

174 linical and laboratory parameters monitored, ADMA levels were the strongest independent predictor of

175 Neither ADMA nor homocysteine correlated with the presence or ex

176 solute synthesis rate (ASR) and reduced NOx, ADMA, and SDMA concentrations.

177 We also found that in the absence of ADMA, eNOS translocation decreased mitochondrial oxygen

178 tochondrial redistribution in the absence of ADMA.

179 se demonstrated tubular cell accumulation of ADMA and lower NO concentrations, but unaltered plasma A

180 of DDAH-1 activity leads to accumulation of ADMA and reduction in NO signaling.

181 determine the free energies of activation of ADMA and SDMA synthesis.

182 The addition of ADMA reduced NOx and increased H2 O2 levels (p<0.001).

183 ice, and cultured aortas released amounts of ADMA to similar to controls.

184 trol subjects, we observed higher amounts of ADMA-degradation enzyme dimethylarginine dimethylaminohy

185 thylaminohydrolase-1 (but similar amounts of ADMA-producing enzyme, protein methyltransferase-1) in t

186 se findings indicate that the association of ADMA level with the risk of CKD progression is modified

187 as for l-arginine and L-NMMA, the binding of ADMA shifts the eNOS heme to the high-spin state, indica

188 Concentrations of ADMA are controlled by two isoforms of its catabolic enz

189 se (DDAH), which catalyzes the conversion of ADMA to citrulline.

190 e more resistant to the inhibitory effect of ADMA on angioadaptation (angiogenesis and arteriogenesis

191 es we measured the dose-dependent effects of ADMA and L-NMMA on (*)O 2 (-) production from eNOS under

192 Therefore, the dose-dependent effects of ADMA and L-NMMA on eNOS function were determined.

193 dium also reversed the inhibitory effects of ADMA and N(G)-nitro-l-arginine methyl ester on inducible

194 The effects of ADMA on endothelial permeability, Rac1 activation and VA

195 n current study, we evaluated the effects of ADMA on gene expression and metabolism in serum-starved

196 TG animals were resistant to the effects of ADMA on neovascularization.

197 proposed to inhibit the catabolic enzyme of ADMA, dimethylarginine dimethylaminohydrolase (DDAH), bu

198 Levels of ADMA and C-reactive protein (CRP) were assessed with a c

199 ese results suggest that increased levels of ADMA and mitochondrial changes may contribute to impaire

200 e-2(-/-) mice had increased plasma levels of ADMA and monomethyl-l-arginine and reduced endothelial n

201 erase 2 (AGXT2) regulates systemic levels of ADMA and SDMA, and also of beta-aminoisobutyric acid (BA

202 Increased plasma levels of ADMA are associated with endothelial vasodilator dysfunc

203 NO synthesis, and elevated plasma levels of ADMA are associated with poor outcomes.

204 temic vascular resistance, whereas levels of ADMA correlated with pulmonary capillary wedge pressure

205 nts were also found to have higher levels of ADMA in the skeletal muscle.

206 and activity, and elevated plasma levels of ADMA, SDMA and BAIB, compared to wild-type littermates.

207 dothelial DDAH1 accounts for the majority of ADMA metabolism.

208 To induce systemic overburden of ADMA, Tg-SwDI mice were treated with a daily dose of exo

209 this study was to assess the relationship of ADMA and homocysteine to subclinical vascular disease in

210 interest in this pathway and in the role of ADMA as a cardiovascular risk factor, there is little ev

211 little evidence to support a causal role of ADMA in pathophysiology.

212 l, these data document the potential role of ADMA in the cognitive pathology under conditions of cere

213 The role of ADMA in the pathogenesis of childhood SM is unknown.

214 We studied the role of ADMA, and the enzymes metabolizing it, dimethylarginine

215 ed by DDAH-1, which is expressed at sites of ADMA metabolism in the kidney cortex and liver, whereas

216 tate turnover reactions of DDAH with NMMA or ADMA.

217 t all sites, but were unchanged with pacing (ADMA, p = 0.5; sCD40L, p = 0.8) or in control patients (

218 .5; sCD40L, p = 0.8) or in control patients (ADMA, p = 0.6; sCD40L, p = 0.9).

219 Plasma ADMA and SDMA were significantly higher in alcoholic hep

220 Plasma ADMA levels were associated with subsequent development

221 Plasma ADMA was approximately 40% lower in DDAH1 Tg mice compar

222 Plasma ADMA was unchanged in DDAH1(En-/-) mice, and cultured ao

223 In contrast to adults, plasma ADMA is reduced in SM in children, but hypoargininemia i

224 val] =2.72 [1.06-6.94]; P=0.038), and plasma ADMA levels greater than 0.70 micromol/L most accurately

225 modifier of the relationship between plasma ADMA level and renal events (doubling of baseline serum

226 in multiple organ systems determines plasma ADMA concentrations.

227 We find that PPIs elevate plasma ADMA levels and reduce nitric oxide levels and endotheli

228 Elevated plasma ADMA is associated with coronary intimal hyperplasia, su

229 Elevated plasma ADMA is associated with increased risk for cardiovascula

230 MV DNA-positive leukocytes had higher plasma ADMA concentrations and more extensive transplant arteri

231 There was a significant reduction in plasma ADMA concentrations following statin therapy compared wi

232 CTs showed a significant reduction in plasma ADMA concentrations following therapy with hydrophilic s

233 se-2 inhibitors also showed increased plasma ADMA.

234 In vivo administration increases plasma ADMA levels, giving proof of concept that these inhibito

235 al DDAH1 mRNA transcription and lower plasma ADMA levels, but counterintuitively, a steeper rate of r

236 late-onset asthma had a higher median plasma ADMA level (0.48 muM, [interquartile range (IQR), 0.35-0

237 DAH1 is not a critical determinant of plasma ADMA, vascular reactivity, or hemodynamic homeostasis.

238 investigate the effect of statins on plasma ADMA concentrations.

239 In DDAH-I recipients, plasma ADMA concentrations were lower, in association with redu

240 with chronic heart failure subjects, plasma ADMA was significantly higher (median [interquartile ran

241 Our previous study reveals the plasma ADMA level is elevated in colon cancer patients, which c

242 ower NO concentrations, but unaltered plasma ADMA concentrations.

243 herosclerosis closely correlated with plasma ADMA levels in male but not female mice fed either a sta

244 d analyses); the risk associated with raised ADMA levels was highest in patients with low FGF-23 leve

245 hylarginine-metabolizing enzyme that reduces ADMA levels.

246 rtance of DDAH1 and MED23/Arg1 in regulating ADMA and l-arginine metabolism, respectively, and identi

247 S(ADMA) was increased only after siDDAH-1 (266+/-25 versus

248 whether DDAH-1 or -2 regulates serum ADMA (S(ADMA)) and/or endothelium-derived relaxing factor (EDRF)

249 In conclusion, S(ADMA) is regulated by DDAH-1, which is expressed at site

250 odel, the significant predictors of salivary ADMA levels were hs-CRP (P < 0.001) and education socioe

251 ay thiols, including homocysteine, and serum ADMA and SDMA concentrations at population level.

252 resented higher levels of salivary and serum ADMA compared to healthy subjects and CP patients.

253 nt predictor of increased salivary and serum ADMA levels.

254 th diseases (CP + CHD) on salivary and serum ADMA levels.

255 entile) concentrations of salivary and serum ADMA were significantly higher in the CHD group [serum:

256 RP remained a significant predictor of serum ADMA (P < 0.001).

257 ric oxide levels through modulation of serum ADMA levels via direct regulation of hepatic DDAH1 gene

258 The level of serum ADMA was reduced concomitantly.

259 dication exposure, C-reactive protein, serum ADMA and SDMA (LC-MS/MS), and thiols (homocysteine, cyst

260 tested whether DDAH-1 or -2 regulates serum ADMA (S(ADMA)) and/or endothelium-derived relaxing facto

261 01) were significantly associated with serum ADMA, whereas in a multivariate model, hs-CRP remained a

262 t the hypothesis that reduced renal-specific ADMA metabolism protects against progressive renal damag

263 In prospective clinical studies, ADMA has been characterized as a cardiovascular risk mar

264 for increased methylarginines and subsequent ADMA-mediated endothelial nitric-oxide synthase impairme

265 study, we investigated the role of systemic ADMA overburden in cerebromicrovascular pathology associ

266 ss conditions, leading many to conclude that ADMA accumulation occurs via increased synthesis by PRMT

267 MA uptake studies demonstrated that ADMA and L-NMMA accumulate in endothelial cells with int

268 We tested the hypothesis that ADMA and FGF23 are interactive factors for CKD progressi

269 It was hypothesized that ADMA concentrations may influence CAV progression during

270 Our findings provide proof-of-principle that ADMA plays a causal role as a culprit molecule in athero

271 We show that ADMA increases pulmonary endothelial permeability in vit

272 findings demonstrate for the first time that ADMA metabolism critically determines pulmonary endothel

273 primary methyltransferase that deposits the ADMA mark, and it accounts for over 90% of this type of

274 rrelates of arterial stiffening included the ADMA concentration, the presence of diabetes mellitus, o

275 that overexpress the human isoform 1 of the ADMA degrading enzyme DDAH into ApoE-deficient mice to g

276 ng mice transgenic for overexpression of the ADMA-hydrolyzing enzyme dimethylarginine dimethylaminohy

277 l-citrulline prevented the ADMA-mediated increase in nitrotyrosine in HBECs in cell

278 pharmacological interventions targeting the ADMA/DDAH pathway may represent a novel approach in the

279 l methylarginine metabolism, and therapeutic ADMA reduction may even be deleterious to kidney functio

280 diated by its reduction of plasma and tissue ADMA concentrations.

281 re associated with reduced plasma and tissue ADMA levels and enhanced tissue NOS enzyme activity.

282 sed DDAH activity, reduced plasma and tissue ADMA levels, increased nitric oxide synthesis, and reduc

283 ma phenotype, plasma ratios of L-arginine to ADMA may explain the inverse relationship of BMI to Fe(N

284 The L-arginine level and the L-arginine to ADMA ratio (a measure of L-arginine bioavailability) wer

285 spectively [P = .0001]; median L-arginine to ADMA ratio, 115, 125, and 187, respectively [P = .0001])

286 8) and was associated with the L-arginine to ADMA ratio.

287 e of pulmonary arterial endothelial cells to ADMA enhanced eNOS phosphorylation at the Akt1-dependent

288 data demonstrate that reduced renal tubular ADMA metabolism protects against progressive kidney func

289 and nifedipine did not affect plasma urate, ADMA, or urine ET-1/creatinine, which reflects renal ET-

290 rms that MMA and SDMA levels accumulate when ADMA levels are reduced.

291 n brain microvessel endothelial cells, where ADMA in the presence of VEGF-induced endothelial cell si

292 ession and metabolism of LoVo cells, whereas ADMA could restore most of the changes at transcriptiona

293 Our study assessed whether ADMA, and its stereo-isomer symmetric dimethylarginine (

294 t and positive independent associations with ADMA and SDMA.

295 uble dagger) = 3.2 kcal/mol as compared with ADMA) may explain the small amount of SDMA generated by

296 1) than cirrhosis alone, and correlated with ADMA measurement.

297 Treatment of C2C12 myotubes with ADMA impaired protein synthesis and reduced mitochondria

298 y separated with control cells, but not with ADMA-treated cells in PCA model.

299 degree of enhancement as that observed with ADMA.

300 e shown to be the preferred substrates, with ADMA displaying a slightly higher k(cat)/K(M) value than