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 is metabolized by the enzyme dimethylarginine dimet

6 ADMA levels are controlled by dimethylarginine dimethyla

7 ADMA remained the only independent predictor of mortalit

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

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

10 ADMA-induced remodeling of actin cytoskeleton and interc

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

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

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

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

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

16 aracterized by elevations in plasma ET-1 and ADMA levels that may contribute to alterations in cutane

17 ficant negative correlation between ET-1 and ADMA values and measures of microvascular perfusion but

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

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

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

21 2) and increased markers of inflammation and ADMA.

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

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

24 DAH I expression, measurement of lung NO and ADMA content, and in vitro assay of DDAH enzyme activity

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 In the absence of L-arginine, ADMA (1 microm) inhibited O(2)(.) generation by approxim

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

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

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

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

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

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

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

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

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

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

42 ncreasing the plasma and myocardial arginine:ADMA ratio.

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

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

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

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

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

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

49 1 active site enables PRMT1 to generate both ADMA and SDMA.

50 NOx FSR inversely correlated with both ADMA and SDMA.

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

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

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

54 dimethylaminohydrolase 2, which catabolizes ADMA.

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

56 assess the effect of statins on circulating ADMA levels.

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

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

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

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

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

62 thylaminohydrolase, the enzyme that degrades ADMA.

63 Under conditions of BH(4) depletion, ADMA had no effect on O(2)(.), whereas L-NMMA increased

64 Asymmetric dimethylarginine (ADMA) and homocysteine are mechanistically interrelated

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

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

67 methylarginines asymmetric dimethylarginine (ADMA) and N(G)-monomethyl-L-arginine (L-NMMA) regulate n

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

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

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

71 23 (FGF-23) and asymmetric dimethylarginine (ADMA) are associated with progression of CKD.

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

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

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

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

76 Asymmetric dimethylarginine (ADMA) is an endogenous metabolite.

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

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

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 of nitric oxide synthase,

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

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

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

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

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

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

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

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

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

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

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

94 helin 1 (ET-1), asymmetric dimethylarginine (ADMA), intercellular adhesion molecule 1, vascular cell

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 PRMT, producing asymmetric dimethylarginine (ADMA).

98 thase inhibitor asymmetric dimethylarginine (ADMA).

99 (NOS) inhibitor asymmetric dimethylarginine (ADMA).

100 e and increased asymmetric dimethylarginine (ADMA).

101 We focused on asymmetric dimethylarginine (ADMA, the endogenous inhibitor of nitric oxide synthase)

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

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

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

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

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

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

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

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

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

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

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

113 Elevated ADMA and diminished global arginine bioavailability rati

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 the elaboration and metabolism of endogenous ADMA plays an important role in regulation of NOS activi

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

118 investigate the significance of endothelial ADMA in cardiovascular homeostasis.

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 nsplant recipients is associated with higher ADMA elevation and more severe TA.

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

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 sed DDAH activity and the subsequent fall in ADMA could contribute to the positive effect of estrogen

146 The increase in ADMA was temporally associated with a reduction in the a

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

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

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

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

151 ntracellular ADMA accumulation and increased ADMA-induced mitotoxicity.

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

153 Consequently, increased ADMA is associated with cardiovascular disease.

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

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

156 stress, impairs DDAH activity, and increases ADMA elaboration.

157 Increasing ADMA reduces NO formation and increases oxidative and ni

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

159 ulmonary concentrations of the NOS inhibitor ADMA.

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

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

162 y producer of the competitive NOS inhibitor, ADMA.

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

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

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

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

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

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

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

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

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

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

173 We hypothesized that lowering ADMA concentrations by dimethylarginine dimethylaminohyd

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

175 hydrolase (DDAH, the enzyme that metabolizes ADMA).

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

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

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

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

180 fected with the CMV isolates elaborated more ADMA.

181 Neither ADMA nor homocysteine correlated with the presence or ex

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

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

184 tochondrial redistribution in the absence of ADMA.

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

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

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

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

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

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

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

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

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

194 The concentration of ADMA in the plasma of 15 postmenopausal women was 0.722+

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

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

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

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

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

200 e, we measured the dose-dependent effects of ADMA and L-NMMA on the rate and amount of O(2)(.) produc

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

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

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

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

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

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

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

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

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

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

211 perfusion had significantly higher levels of ADMA than did women with normal doppler waveforms (2.4 m

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

213 dothelial DDAH1 accounts for the majority of ADMA metabolism.

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

215 gens can alter the catabolism and release of ADMA in vitro and reduce the circulating concentration i

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

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

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

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

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

221 tate turnover reactions of DDAH with NMMA or ADMA.

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

223 .5; sCD40L, p = 0.8) or in control patients (ADMA, p = 0.6; sCD40L, p = 0.9).

224 Plasma ADMA and SDMA were significantly higher in alcoholic hep

225 Plasma ADMA levels were associated with subsequent development

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

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

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

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

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

231 in multiple organ systems determines plasma ADMA concentrations.

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

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

234 Elevated plasma ADMA is associated with increased risk for cardiovascula

235 splant recipients manifested elevated plasma ADMA levels compared with healthy control subjects.

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

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

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

239 associated with a 2-fold reduction in plasma ADMA.

240 se-2 inhibitors also showed increased plasma ADMA.

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

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

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

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

245 investigate the effect of statins on plasma ADMA concentrations.

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

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

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

249 ower NO concentrations, but unaltered plasma ADMA concentrations.

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

251 by 37% and 22%, respectively), but pulmonary ADMA concentrations were increased by 2.3-fold compared

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

253 hylarginine-metabolizing enzyme that reduces ADMA levels.

254 lase (DDAH), the activity of which regulates ADMA concentrations and provides a mechanism for modulat

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

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

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

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

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

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

261 The level of serum ADMA was reduced concomitantly.

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

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

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

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

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

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

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

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

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

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

272 We show that ADMA increases pulmonary endothelial permeability in vit

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

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

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

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

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

278 ced pulmonary expression and activity of the ADMA-metabolizing enzyme DDAH I.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

295 t and positive independent associations with ADMA and SDMA.

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

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

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