ライフサイエンスコーパス: NOS inhibitor

1 L-arginine methyl ester (L-NAME), a specific NOS inhibitor.

2 ase inhibition was lost in the presence of a NOS inhibitor.

3 Arginine-induced coupling was abolished by a NOS inhibitor.

4 ancing effects was tested with the use of an NOS inhibitor.

5 rginine methyl ester (L-NAME), a competitive NOS inhibitor.

6 e NOS active site suggests novel designs for NOS inhibitors.

7 eproduced in WT corpus cavernosum exposed to NOS inhibitors.

8 OS and DNA breaks, which could be blocked by NOS inhibitors.

9 -/- or NOS3-/-) mice or in mice treated with NOS inhibitors.

10 was used to evaluate a series of established NOS inhibitors.

11 on and investigated its ability to transport NOS inhibitors.

12 rt a broad range of zwitterionic or cationic NOS inhibitors.

13 abotropic glutamate receptor antagonists and NOS inhibitors.

14 taglandin biosynthesis to the same extent as NOS inhibitors.

15 he steroid dexamethasone was not affected by NOS inhibitors.

16 ine are key pharmacophores for this class of NOS inhibitors.

17 icity in the presence of either NO donors or NOS inhibitors.

18 ere markedly attenuated by VEGF antibody and NOS inhibitors.

19 nNOS has not been determined using selective NOS inhibitors.

20 he future fragment-based design of selective NOS inhibitors.

21 e report here a cellular model for screening NOS inhibitors.

22 DDAH), an enzyme that catabolizes endogenous NOS inhibitors.

23 on of a non-selective nitric oxide synthase (NOS) inhibitor.

24 the syntheses of four nitric oxide synthase (NOS) inhibitors.

25 (18)F-radiolabeled analog of the reversible NOS inhibitor, 2-amino-4-methylpyridine ((18)F-NOS), and

26 y of a novel class of nitric oxide synthase (NOS) inhibitors, 2-substituted 1,2-dihydro-4-quinazolina

27 rginine methyl ester (L-NAME), a nonspecific NOS inhibitor, 25 mg/kg of 7-nitroindazole (7-NI), a sel

28 ne methyl ester hydrochloride (non-selective NOS inhibitor); (3) 5 mm N-propyl-l-arginine (nNOS inhib

29 ne-methyl-ester (-NAME), the specific neural NOS inhibitor 7-nitroindazole (7-NI), or Ang II individu

30 To test the involvement of NO, we used the NOS inhibitors 7-nitroindazole and L-nitroarginine.

31 The nitric-oxide synthase (NOS) inhibitors 7-nitroindazole (7-NI) and N-omega-nitro

32 ether APC could be inhibited by NO synthase (NOS) inhibitor (7-nitroindazole).

33 inhibition of eNOS by RNA interference or by NOS inhibitor abolished the blocking effect of kallistat

34 rent was enhanced by the same treatment, and NOS inhibitors abolished both the elevation of NO and th

35 Exposure of mouse bladder to small molecule NOS inhibitors abrogates infection of the uroepithelium

36 d spinal cord, has both NMDAR antagonist and NOS inhibitor activities.

37 In the presence of NOS inhibitors, additional Ca(2+) influx occurs through

38 th increased pulmonary concentrations of the NOS inhibitor ADMA.

39 animals were treated with either PBS or the NOS inhibitors ADMA or N(omega)-nitro-L-arginine methyl

40 t is the primary producer of the competitive NOS inhibitor, ADMA.

41 Neither NO donors nor NOS inhibitors affected GCDC-induced mitochondrial perme

42 and ICAM-1 or inducible NOS expression, the NOS inhibitor almost completely inhibited expression of

43 strain endotoxemic mice co-administered the NOS inhibitor aminoguanidine.

44 cts were prevented by nitric oxide synthase (NOS) inhibitors (aminoguanidine and N(G)-monomethyl L-ar

45 d computational approach to isozyme-specific NOS inhibitor analysis and design.

46 both cardiac-specific genes with nonspecific NOS inhibitor and a concomitant increase and decrease in

47 which are diminished by NMDA antagonists and NOS inhibitors and also diminished in mice with targeted

48 In wild-type mice, NOS inhibitors and HO inhibitors partially inhibited non

49 XO and NOS inhibitors and NOS-3 KO mice injected with LPS had d

50 ated NO synthesis that could be inhibited by NOS inhibitors and quenched by a NO scavenger; this NOS

51 could reduce tissue and plasma levels of the NOS inhibitors and thereby increase NO synthesis.

52 vations after administration of NO synthase (NOS) inhibitor and NO donor both regionally and systemic

53 ntly reduced in the presence of NO synthase (NOS) inhibitors and the xanthine oxidase (XO) inhibitor

54 ylyl cyclase (NO-sGC) receptor antagonist, a NOS inhibitor, and NO donors, suggested that NO released

55 se of S-methylisothiourea (SMT), a selective NOS inhibitor, and those of saline.

56 itro assays regarding the bioavailability of NOS inhibitors, and it is suitable for high-throughput s

57 Isothioureas are potent NOS inhibitors, and the structures of the endothelial NO

58 the systemic administration of non-selective NOS inhibitors, and thus provides support for the potent

59 e effects of arginine, nitric oxide sythase (NOS) inhibitors, and NO donors.

60 ro-l-arginine [NLA; a nitric oxide synthase (NOS) inhibitor] and l-arginine (substrate for NO product

61 The majority of existing NOS inhibitors are either based on the structure of argi

62 Isoform-selective NOS inhibitors are highly desirable to regulate the NO p

63 While non-selective NOS inhibitors are neuroprotective, the role of nNOS has

64 te to several pathophysiological conditions, NOS inhibitors are of interest as potential therapeutic

65 In this study, a small set of known NOS inhibitors are surveyed as inhibitors of recombinant

66 Nitric oxide synthase (NOS) inhibitors are potential drug candidates because it

67 0 nmol) as well as by the selective neuronal NOS inhibitor ARL 17477 (30-600 nmol).

68 ping arginine mimetic, substrate-competitive NOS inhibitors as drugs have met with little success.

69 els after treatment with NMDA antagonists or NOS inhibitors, as well as in nNOS(-/-) mice, indicates

70 d pulmonary concentrations of the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA) in the

71 h our recent work implicating the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA), a card

72 The NOS inhibitors asymmetric dimethylarginine (ADMA) and N-

73 els of the endogenous nitric oxide synthase (NOS) inhibitor asymmetric dimethylarginine (ADMA).

74 hesis of NO by treatment with a NO synthase (NOS) inhibitor attenuates spontaneous migraine headaches

75 oduced only short-term potentiation, whereas NOS inhibitors blocked LTP to stimuli that normally prod

76 by specific inducible (i)NOS or neuronal (n)NOS inhibitors, blunted IPC and IPC-mimicking, as did bl

77 -arginine (L-NMMA), a nitric oxide synthase (NOS) inhibitor; BQ-788, an ET receptor B (ETB) antagonis

78 esence of L-NG-monomethyl arginine (L-NMMA) (NOS inhibitor) but not of D-NG-monomethyl arginine (D-NM

79 was attenuated in a stereospecific manner by NOS inhibitors, but these compounds did not inhibit TCR-

80 cture-based design and synthesis of a unique NOS inhibitor, called nanoshutter NS1, with two-photon a

81 NOS inhibitors completely blocked agrin-induced AChR agg

82 Treatment of H-2Kb cells or rat muscle with NOS inhibitors completely blocks the increase in glucose

83 sis from L-arginine), which were affected by NOS inhibitors confirming the presence of functional enz

84 Conversely, N(G)-monomethyl-L-arginine, a NOS inhibitor, decreased PPARgamma binding.

85 re, the treatment with TNF-alpha, as well as NOS inhibitors, decreased interferon-gamma-induced S-nit

86 2)) brain toxicity as nitric oxide synthase (NOS) inhibitors delay latent time before the onset of se

87 as a template for next generation selective NOS inhibitor design but also opens new prospects for th

88 site and identify an important constraint on NOS inhibitor design.

89 tetrahydroquinoline-based selective neuronal NOS inhibitors due to higher lipophilicity.

90 factor nuclear factor kappaB (NF kappaB) as NOS inhibitors enhance basal NF kappaB activation.

91 iven i.p. 20 and 4 h prior to MPTP), another NOS inhibitor, failed to affect MPTP-induced ATP depleti

92 We conclude that nitric oxide synthase (NOS) inhibitors, given as a single large bolus in the ea

93 In contrast, NOS inhibitors had no effect on GCDC-induced apoptosis d

94 Pretreatment with L-NAME, a nonselective NOS inhibitor, had no effect on Akt and eNOS phosphoryla

95 Combination of CA-4-P with a NOS inhibitor has an additive effect, which it may be po

96 mmatory, and autoimmune disorders, design of NOS inhibitors has received much attention.

97 sults from normal animals indicate that both NOS inhibitors have adverse effects on cardiac function

98 O levels should be beneficial in sepsis, but NOS inhibitors have had a checkered history in animal mo

99 For example, nitric oxide synthase (NOS) inhibitors have been suggested as antitumor therape

100 Nitric oxide synthase (NOS) inhibitors have therapeutic potential in the manage

101 isk angiogenesis system was impaired by both NOS inhibitors; however, TG animals were resistant to th

102 G) -nitro-l-arginine (l-NNA), a non-specific NOS inhibitor; (iii) 50 mm tetraethylammonium (TEA), a n

103 amine the effects of an isoform-nonselective NOS inhibitor in patients with MI and refractory cardiog

104 rtunity for the use of NMDAR antagonists and NOS inhibitors in chronic pain.

105 an ion gradient-driven transport system for NOS inhibitors in the intestinal tract.

106 ard to the therapeutic use of methylarginine-NOS inhibitors in the treatment of disease.

107 tic use of l-arginine and the methylarginine-NOS inhibitors in the treatment of disease.

108 then studied transport of a wide variety of NOS inhibitors in Xenopus laevis oocytes expressing the

109 onomethyl-L-arginine (L-NMMA), a nonspecific NOS inhibitor, in three models of ocular neovascularizat

110 Both NOS inhibitors increased MAP but decreased RBF, but only

111 NG-nitro-L-arginine methyl ester (L-NAME, a NOS inhibitor), increased submaximal tetanic and peak tw

112 systemic infusion of nitric oxide synthase (NOS) inhibitors increases blood pressure due to inhibiti

113 e (MAP), while the injection of NO synthase (NOS) inhibitors increases MAP.

114 hile the injection of nitric oxide synthase (NOS) inhibitors increases MAP.

115 Second, L-nitroarginine (L-NA), an NOS inhibitor, increases the rate of the heartbeat (oppo

116 ings showing that the nitric oxide synthase (NOS) inhibitor-induced repression of the CO2 response co

117 ctivity for this class of cyclic amidines as NOS inhibitors is described.

118 the intestine that can mediate the uptake of NOS inhibitors is important to assess the oral bioavaila

119 g TG2(-/-) mice chronically treated with the NOS inhibitor l-N(G)-nitroarginine methyl ester (L-NAME)

120 d colon enterocytes of infected animals; the NOS inhibitor L-N-iminoethyl lysine or N-nitro-L-arginin

121 tric oxide synthase (eNOS) with the specific NOS inhibitor L-NAME (N(G)-nitro-l-arginine methyl ester

122 NOS inhibitor L-NAME also significantly attenuated RGS4

123 This effect was inhibited by the NOS inhibitor l-NAME and was not seen when astrocytes we

124 s observed which could not be blocked by the NOS inhibitor L-NAME but was blocked by the arginase inh

125 The NOS inhibitor L-NAME normalized pressure-dependent drain

126 electrical stimulation, is prevented by the NOS inhibitor L-NAME or in nNOS-deleted mice.

127 and simultaneous treatment of cells with the NOS inhibitor L-NAME resulted in telomere elongation and

128 Administration of the NOS inhibitor l-NAME to pregnant mice recapitulated the

129 The NOS inhibitor L-NAME, the NO scavenger PTIO, the sGC inh

130 C4 nuclear translocation is prevented by the NOS inhibitor l-NAME.

131 his dilatation was partially reversed by the NOS inhibitor l-NAME.

132 r, both cells were equally suppressed by the NOS inhibitor l-NAME.

133 Rats treated with the non-isoform-specific NOS inhibitor L-nitro-arginine methyl ester during 3 wee

134 be completely prevented by the nonselective NOS inhibitor L-nitroarginine (3 mmol/L) or the specific

135 nor pentaerythritol tetranitrate (PETN), the NOS inhibitor l-nitroarginine (L-NA), plasma pool C1-INH

136 The NOS inhibitor L-nitroarginine methyl ester is neuroprote

137 ulated by BMP2 and BMP4 was inhibited by the NOS inhibitor l-nitroarginine methyl ester, providing fu

138 Treatment of AD10 cells with the NOS inhibitor l-NMA blocked the IFN-gamma-dependent sens

139 for sanguinarine-induced cell death because NOS inhibitor L-NMMA efficiently protected cells from ap

140 By contrast, the NOS inhibitor L-NMMA significantly reduced basal choroid

141 In the presence of the NOS inhibitors L-NAME, TRIM, or 7-NI, but not the inacti

142 gonist PD 174494, the nitric oxide synthase (NOS) inhibitor L-N(omega)-Nitroarginine methyl ester (L-

143 The nitric oxide synthetase (NOS) inhibitor L-NAME (10 microM) abrogated all effects

144 n the presence of the nitric oxide synthase (NOS) inhibitor l-NAME (10(-5) mol l(-1)) or the combinat

145 FVC that was attenuated by the NO synthase (NOS) inhibitor l-NAME (Group 1, n = 8) and adenosine A1

146 were abrogated by the nitric-oxide synthase (NOS) inhibitor L-NAME (N(D)-nitro-L-arginine methyl este

147 administration of the nitric oxide synthase (NOS) inhibitor L-NAME and in mice with neuronal and indu

148 nce or absence of the nitric oxide synthase (NOS) inhibitor L-NAME.

149 are inhibited by the nitric oxide synthase (NOS) inhibitor L-NIO, and genetic inhibition of endothel

150 dogenous NO production with the NO synthase (NOS) inhibitor L-NMMA causes a significant increase in T

151 phenylephrine or the nitric oxide synthase (NOS) inhibitor L-NMMA may alter the choroidal blood flow

152 Addition of the NO synthase (NOS) inhibitors L-nitro-arginine methylester (L-NAME, 1

153 tely with a sodium channel blocker (TTX), an NOS inhibitor (L-NNA), or a specific inhibitor of neuron

154 microinjection of non-selective NO synthase (NOS) inhibitors (L-NAME; 50 pmol) or (L-NMMA; 200 pmol)

155 ppressed by administering a specific Type II NOS inhibitor [L-N(6)-(1-iminoethyl)-lysine (L-NIL)].

156 mpletely prevented by pre-treatment with the NOS inhibitor, L-N(G)-monomethyl arginine (L-NMMA, 1 mM)

157 00 microg/kg, i.v.) in rats treated with the NOS inhibitor, L-NAME (25 micromol/kg, i.v.) elicited si

158 abolished by systemic administration of the NOS inhibitor, L-NAME, or by bilateral vagotomy.

159 cs and a 5-fold increased sensitivity to the NOS inhibitor, l-NAME.

160 We find that an NOS inhibitor, L-NMMA, blocked regeneration of lymphatic

161 The NOS inhibitor, L-NMMA, blocked VEGF-induced vascular hyp

162 rine (5 microM), or a nitric oxide synthase (NOS) inhibitor, l-nitro(G)-arginine methyl ester (l-NAME

163 afil was inhibited by nitric-oxide synthase (NOS) inhibitor, L-nitro-amino-methyl-ester.

164 Both NOS inhibitors led to left ventricular dilation, but PE

165 NOS inhibitors LNNA, SMT, and 7NI significantly attenuat

166 Isoform-specific nitric-oxide synthase (NOS) inhibitors may prove clinically useful in reducing

167 Treating the cells with the broad NOS inhibitor N(G)-methyl-l-arginine, the free radical s

168 The nonselective NOS inhibitor N(G)-monomethyl-L-arginine (25 micromol/mi

169 icular and VMH injection of the nonselective NOS inhibitor N(G)-monomethyl-l-arginine (l-NMMA) slowed

170 nalaprilat (0.2 mg/min) with and without the NOS inhibitor N(G)-monomethyl-L-arginine (L-NMMA, 5 mg/m

171 Topical superfusion of the nonselective NOS inhibitor N(G)-monomethyl-L-arginine (NMA) on skelet

172 onverted L-arginine to L-citrulline, but the NOS inhibitor N(G)-monomethyl-L-arginine (NMMA) inhibite

173 ibition of NOS activity with the nonspecific NOS inhibitor N(G)-monomethyl-L-arginine or by the antio

174 nificant bradycardia (68+/-14 bpm) while the NOS inhibitor N(G)-nitro-l-arginine (l-NNA) (3 mM, 50 nl

175 NOS inhibitor N(G)-nitro-L-arginine (L-NNA) prevented th

176 ion (control), microdialysis delivery of the NOS inhibitor N(G)-nitro-l-arginine (NLA; 10 mm) increas

177 intraperitoneal (i.p.) administration of the NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME

178 g mice treated post-IR with the constitutive NOS inhibitor N(G)-nitro-l-arginine methyl ester (L-NAME

179 ted with L-arginine, D-arginine, nonspecific NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME

180 The NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME

181 e show that extracellular application of the NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME

182 during a 60 min intravenous infusion of the NOS inhibitor N(G)-nitro-l-arginine methyl ester (l-NAME

183 flow were determined in the presence of the NOS inhibitor N(G)-nitro-L-arginine methyl ester (l-NAME

184 The NOS inhibitor N(G)-nitro-l-arginine methyl ester and gen

185 NOS inhibitor N(G)-nitro-L-arginine methyl ester attenua

186 The protective effect of the NOS inhibitor N(G)-nitro-L-arginine methyl ester could b

187 Mice that received the broad-spectrum NOS inhibitor N(g)-nitro-L-arginine methyl ester hydroch

188 Furthermore, using a tritiated analog of the NOS inhibitor N(G)-nitro-L-arginine, we showed that Na+

189 h or leptin was abolished with incubation of NOS inhibitor N(G)-nitro-l-arginine-methyl ester (l-NAME

190 Wild-type mice treated with the NOS inhibitor N(omega)-nitro L-arginine (L-NA) and eNOS-

191 ditioned rabbits were given the nonselective NOS inhibitor N(omega)-nitro-L-arginine (L-NA, 13 mg/kg

192 ecreasing NO synthesis by application of the NOS inhibitor N(w)-nitro-L-arginine methyl ester (1 mM)

193 itroso-N-acetylpenicillamine (SNAP), and the NOS inhibitor N-iminoethyl-L-ornithine (L-NIO), we perfo

194 +/calmodulin and was blocked by the specific NOS inhibitor N-nitro-L-arginine methyl ester (L-NAME) b

195 OS are mimicked by the administration of the NOS inhibitor N-nitro-L-arginine methyl ester hydrochlor

196 uire SOD, and it was blocked by the specific NOS inhibitor N-nitro-L-arginine methyl ester.

197 d circulating EPCs, effects inhibited by the NOS inhibitor N-nitro-L-arginine-methyl ester.

198 The NOS inhibitors N(G)-methyl-L-arginine and aminoguanidine

199 line; 10(-9) to 10(-5) m) was blocked by the NOS inhibitors N(G)-nitro-L-arginine methyl ester (30 mi

200 ibited by both nonspecific and NOS1-specific NOS inhibitors N(G)-nitro-l-arginine methyl ester and S-

201 with the nonselective nitric oxide synthase (NOS) inhibitor N (G)-nitro-L-arginine methyl ester (L-NA

202 regimes and given the nitric oxide synthase (NOS) inhibitor N(6)-nitro-L-arginine methyl ester (L-NAM

203 ered the nonselective nitric oxide synthase (NOS) inhibitor N(G)-L-arginine methyl ester (L-NAME), an

204 ound that administration of the NO synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAM

205 administration of the nitric oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAM

206 g anti-IL-1beta antibody or the NO synthase (NOS) inhibitor N(G)-nitro-L-arginine-methyl ester (L-NAM

207 Addition of the NO synthase (NOS) inhibitor N-monomethyl arginine (NMMA) partially re

208 mice treated with the nitric oxide synthase (NOS) inhibitor N:(G)-nitro-L-arginine (L-NNA), and knock

209 was prevented by the nitric-oxide synthase (NOS) inhibitors N(G)-monomethyl-N-arginine monoacetate (

210 es of MMP-2 activity after the addition of a NOS inhibitor (N(G)-amino-l-arginine) or a (.)NO donor (

211 omoter, and this increase was blocked by the NOS inhibitor (N(G)-monomethyl-L-arginine), but could be

212 Animals were pretreated with a nonselective NOS inhibitor (N(omega)-nitro-L-arginine methyl ester; 3

213 buffer plus either a nitric oxide synthase (NOS) inhibitor (N-monomethyl-L-arginine (NMMA); 300 or 5

214 A NOS inhibitor, N(G)-methyl-l-arginine, enhanced the tumo

215 e untreated or treated for 3 months with the NOS inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAM

216 soglutathione (SNOG), inhibited, whereas the NOS inhibitor, N(G)-nitro-l-arginine methyl ester (L-NAM

217 The NOS inhibitor, N-nitro-L-arginine methyl ester, attenuat

218 Structures of mechanism-based NOS inhibitors, N(5)-(1-iminoethyl)-L-ornithine and N-(3

219 riments were repeated in the presence of the NOS inhibitors, N(G)-nitro-L-arginine methyl ester and a

220 The NOS inhibitors, N-nitro-L-arginine methyl ester, dexamet

221 of the non-selective nitric oxide synthase (NOS) inhibitor, N(G)-nitro-L-arginine (L-NNA) (40 mg/kg)

222 -L-arginine (L-NA), a nitric oxide synthase (NOS) inhibitor, N-2-mercaptopropionyl glycine (MPG), a r

223 In opposite, a nitric oxide synthase (NOS) inhibitor, N-nitro-L-arginine (NNA)(25 mg/kg) decre

224 Treatment with the NO synthase (NOS) inhibitor, N-nitro-l-arginine methyl ester prevente

225 est was the finding that the frequently used NOS inhibitor NG-monomethyl L-arginine enhanced O-2 prod

226 hermore, systemic treatment of mice with the NOS inhibitor NG-monomethyl-l-arginine delayed weight lo

227 -Arg, and decreased with the addition of the NOS inhibitor NG-monomethyl-L-arginine.

228 Addition of the NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME)

229 Systemic administration of the general NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME),

230 wild-type mice treated with the nonspecific NOS inhibitor NG-nitro-L-arginine methyl ester and the N

231 stimulated NO synthesis was inhibited by the NOS inhibitors NG-monomethyl-L-arginine or N-3-aminoethy

232 in E2 (PGE2) with the nitric oxide synthase (NOS) inhibitor NG-methyl-L-arginine (L-NMA) inhibited PG

233 , mice were pretreated with the NO synthase (NOS) inhibitor NG-methyl-L-arginine.

234 with the nonselective nitric oxide synthase (NOS) inhibitor NG-monomethyl-arginine reduced glomerulon

235 mannin (100 nmol/l), and/or the NO synthase (NOS) inhibitor NG-monomethyl-L-arginine (L-NMMA) (0.1 mm

236 n is prevented by the nitric oxide synthase (NOS) inhibitor NG-monomethyl-l-arginine.

237 nistration of the nonselective NO* synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (100-800

238 We now show that the NOS inhibitor, NG-methyl-L-arginine (MLA), also reversib

239 n of nNOS-generated NO* with the competitive NOS inhibitor, NG-nitro-l-arginine methyl ester, in cell

240 mic injection of the nitric oxide synthesis (NOS) inhibitor, NG-nitro-L-arginine methyl ester (L-NAME

241 mechanisms by which a nitric oxide synthase (NOS) inhibitor, NG-nitro-L-arginine methyl ester (L-NAME

242 Luminal application of the nonselective NOS inhibitor nitro-L-arginine (10(-3) and 10(-2) M) enh

243 ty of NOS activation was tested by using the NOS inhibitor nitro-L-arginine methyl ester (L-NAME, 1 m

244 agonist Losartan, the nitric oxide synthase (NOS) inhibitor nitro--arginine-methyl-ester (-NAME), the

245 we examined the effects of the NO synthase (NOS) inhibitor nitro-L-arginine methyl ester (L-NAME).

246 ly by infusion of the nitric oxide synthase (NOS) inhibitor nitro-L-arginine or by the NMDA channel b

247 -diamino6-hydroxy-pyrimidine vs. nonspecific NOS inhibitors (nitro- -arginine-methylester).

248 activity can be blunted by using a specific NOS inhibitor, nitro-l-arginine methyl ester.

249 ne was reached, 1 microM of the nonselective NOS inhibitor NMA was suffused topically followed by phy

250 The NOS inhibitors NMMA, 1400W, and N-iminoethyl-L-lysine ef

251 was abolished by the nitric oxide synthase (NOS) inhibitor NMMA.

252 Supraspinal administration of the NOS inhibitor NOArg lowered both the first and second ph

253 ntravenous administration of the nonspecific NOS inhibitor Nomega-nitro-L-arginine methyl ester (L-NA

254 -selective inhibitor (1400W), a nonselective NOS inhibitor [Nomega-nitro-L-arginine methyl ester (L-N

255 so demonstrated that pretreatment of EC with NOS inhibitor, Nomega-nitro-L-arginine-methyl ester (L-N

256 modulation of the levels of these intrinsic NOS inhibitors offers a novel approach to modulate neuro

257 and examined the effect of a NO donor and a NOS inhibitor on MAP, membrane properties, and synaptic

258 ow was reduced by infusion of a nonselective NOS inhibitor or a high dose of a partially selective in

259 ox/flox); LysMCre(+/-) mice with a selective NOS inhibitor or knockout of Nos2, encoding iNOS, signif

260 ism reversible by ascorbate and inhibited by NOS inhibitors or expression of a dominant negative muta

261 Treatment of HCV-infected cells with NOS inhibitors or small interfering RNA specific for iNO

262 itrite formation with nitric oxide synthase (NOS) inhibitors or a decomposition catalyst did not prev

263 emobilization period, nitric oxide synthase (NOS) inhibitors or substrate were administered.

264 ET-1, 10 mm N(G) -nitro-l-arginine (l-NNA; a NOS inhibitor) or a combination of 400 nm ET-1 and 10 mm

265 7-nitroindazole (7-NI), a selective neuronal NOS inhibitor, or equal volume of vehicle (dimethyl sulf

266 L-NAME, a NOS inhibitor, or saline was injected intraperitoneally

267 is (EAE), it has been shown that nonspecific NOS inhibitors partially ameliorate the disease.

268 N-monomethyl-L-arginine (L-NMA), a NOS inhibitor, partially inhibited NK cell lysis of four

269 ctive behavior, such as penile erection, and NOS inhibitors prevent erection.

270 tment of TNF-alpha mice with antioxidants or NOS inhibitors prevented phosphorylation of C/EBPbeta on

271 Administration of inhaled NO with NOS inhibitors provided more benefits in some conditions

272 er that cytokines and nitric-oxide synthase (NOS) inhibitors regulate S-nitrosation of an initiator c

273 Nitric oxide synthase (NOS) inhibitors rescue this pathology.

274 nTMPyP (a superoxide scavenger) or l-NAME (a NOS inhibitor) reversed their pulmonary vascular patholo

275 Co-administration of the inducible NOS inhibitor S-methylisothiourea or the proteasome inhi

276 In nNOSDelta/Delta animals, NOS inhibitors selectively lost their efficacy, and HO i

277 wed that the most important determinants for NOS inhibitor selectivity are hydrophobic and charge-cha

278 In contrast, dietary provision of a NOS inhibitor significantly increased parasite numbers i

279 tter understanding of the in vivo effects of NOS inhibitors such as AG.

280 tonin do not completely mimic those of other NOS inhibitors, suggesting that the effects of melatonin

281 Previously, we demonstrated that a NOS inhibitor targeting both the active and pterin sites

282 Each of the NOS inhibitors tested compete with glycine for uptake th

283 ted the hypothesis that administration of an NOS inhibitor to the basal forebrain would alter basal f

284 mplex components dE2F and dDP) combined with NOS inhibitors to address this issue.

285 In contrast, a neurone-specific NOS inhibitor, TRIM (50 pmol), was without effect.

286 Neuronal NOS inhibitors verified that CCh responses reflected eNO

287 When a NOS inhibitor was given with rmIL-12 during vaccination

288 Preinjection with an NOS inhibitor was partially protective.

289 When a NO synthase (NOS) inhibitor was used to block NO production, decrease

290 nopentyl)-N'-nitroguanidine, TFA, a neuronal NOS inhibitor, was injected at 0.02 or 0.1 mg/100 microl

291 NAME), a nonselective nitric-oxide synthase (NOS) inhibitor, was injected at 0.02 or 0.2 mg/100 micro

292 osensor NO measurements, and an NO synthase (NOS) inhibitor, we found that NO mediates mural cell cov

293 nal isoform selective nitric oxide synthase (NOS) inhibitors, we have developed a series of compounds

294 NOS inhibitors were protective against this toxicity.

295 NO donors and NOS inhibitors were without effect on long-term depressi

296 New nitric oxide synthase (NOS) inhibitors were designed de novo with knowledge gat

297 P)H autofluorescence was also sensitive to a NOS inhibitor, whereas NOS inhibition did not affect the

298 androgenized individuals were treated with a NOS inhibitor, which eliminated male-like behavior in ha

299 is were examined by comparing the effects of NOS inhibitors with other inhibitors of GCDC-induced apo

300 We tested a few NOS inhibitors with this assay and found that the method