ライフサイエンスコーパス: L-NAME

1 L-NAME (200 micro g/5 micro l), an inhibitor of NO synth

2 L-NAME (N(omega)-nitro-L-arginine methyl ester; nitric o

3 L-NAME abolished this protection (281 +/- 14 mm3; P < 0.

4 L-NAME administered i.c.v. decreased 24 h energy intake

5 L-NAME and SNAP did not affect Rho kinases and ERK1/2 ac

6 L-NAME decreased IOP from 20.8 +/- 1.7 to 16.7 +/- 1.8 m

7 L-NAME decreased sO2 in L and JZ+D at GD14 and GD18 in a

8 L-NAME did not affect ET-1 release.

9 L-NAME impaired the learning of negative patterning but

10 L-NAME increased in situ late distal nephron HCO(3) deli

11 L-NAME increased mean arterial pressure by approximately

12 L-NAME induced generation of neutrophil-derived micropar

13 L-NAME induced hypertrophy (weight-indexed left-ventricu

14 L-NAME may attenuate ventilator-induced microvascular le

15 L-NAME reduced steady-state exercise hyperaemia by 12 +/

16 L-NAME salt-induced hypertension accelerated mesangial c

17 L-NAME significantly reduced body weight gain in DIO but

18 L-NAME was chosen to study an inhibitor that is not degr

19 L-NAME was infused after the established plateau in all

20 L-NAME, a NOS inhibitor, or saline was injected intraper

21 L-NAME-treated animals had significantly fewer TUNEL-pos

22 L-NAME/high salt increased macrophage and dendritic cell

23 G-catalase 82.1+/-2.8; BIBR-1532 69.9+/-4.0, L-NAME 84.7+/-2.2, PEG-catalase 36.5+/-6.9*).

24 diameter at 100 cm H2O: vehicle 74.6+/-4.1, L-NAME 37.0+/-2.0*, PEG-catalase 82.1+/-2.8; BIBR-1532 6

25 es (control, 37.0 +/- 0.3 degrees C, n = 16; L-NAME, 39.8 +/- 0.1 degrees C, n = 4; P < 0.001) and ab

26 In group 2, L-NAME lowered EVP from 11.5 +/- 1.2 to 8.8 +/- 1.0 mm H

27 on before IR, 4) L-arginine before IR, or 5) L-NAME + IPC before IR.

28 In contrast to untreated C57Bl/6, L-NAME decreased placental sO2 at GD14 and GD18 vs GD10

29 at 100 cm H2O: adipose, AGS 499 78.5+/-3.9; L-NAME 10.9+/-17.5*; PEG-catalase 79.2+/-4.9).

30 In addition, L-NAME at a high dose, but not (4S)-N-(4-Amino-5[aminoet

31 After L-NAME, thrombin decreased VWF staining in young aortas.

32 Acute hypoxia after L-NAME still reduced baseline FVR and depressed evoked r

33 e were similar in all groups before or after L-NAME inhibition.

34 etic resonance at baseline and 7 weeks after L-NAME treatment or up to 7 weeks after TAC.

35 duced exocytosis in young (VWF) but not aged L-NAME-treated aortas (VWF, ET-1).

36 at was suppressed by vagal stimulation in an L-NAME-sensitive manner.

37 independent treatments (N-acetylcysteine and L-NAME) that decrease nitration of cardiac proteins led

38 Two sites were pretreated with both BT and L-NAME.

39 1.9- and 1.8-fold higher in the control and L-NAME + pGz groups, respectively, compared with pGz-tre

40 nificant differences between the control and L-NAME conditions for baseline .VO2 (means +/- S.E.M. 79

41 h were abolished by superoxide dismutase and L-NAME, indicating that protein radical formation was du

42 It is interesting that both high glucose and L-NAME enhanced the proliferative response of endothelia

43 nistration of propranolol, indomethacin, and L-NAME.

44 (P < 0.001) inhibited both IL-8-induced and L-NAME enhanced migration.

45 as inhibited by pretreatment with norBNI and L-NAME.

46 om air-exposed rats, N(2)O-exposed rats, and L-NAME-pretreated, N(2)O-exposed rats; they were then an

47 nase signalling following TP stimulation and L-NAME regulates endothelial cell K(Ca)2.3 function.

48 groups were given N(omega)-nitro-L-arginine (L-NAME) (15 mg/kg/day) in drinking water, and the fourth

49 Furthermore, high glucose as well as L-NAME stimulated VEGF and kinase-insert domain receptor

50 differences in CNV size and leakage between L-NAME- and saline-treated groups.

51 wever, this protection was abolished by both L-NAME and 5-hydroxydecanoate.

52 /- 4% decrease in CVC at the L-NAME and BT + L-NAME sites (P < 0.05); subsequent slow LC (34-24 degre

53 Importantly, CVC at the BT + L-NAME sites was unaffected by LC (P > 0.05).

54 change (P > 0.05) at sites treated with BT + L-NAME only.

55 was lower than in N rats breathing air, but L-NAME had qualitatively similar effects on baseline FVR

56 ion in the distal nephron of HiPro rats, but L-NAME had no additive effect on either component.

57 discrimination learning was not affected by L-NAME.

58 administration and was minimally affected by L-NAME.

59 oked by adenosine infusion was attenuated by L-NAME but restored by infusion of NO donor.

60 ose responses are significantly augmented by L-NAME (3-fold for ERK and 4-fold for COX-2).

61 low SS than under high SS, was augmented by L-NAME under high SS and decreased by SNAP under low SS

62 Both events were blocked by L-NAME (N(G)-nitro-L-arginine methyl ester, 3-30 mg/kg),

63 he inhibition of EC insulin uptake caused by L-NAME, wortmannin, the Src inhibitor PP1, and tumor nec

64 phy, fibrosis, and vascular damage caused by L-NAME/Ang II.

65 saline infusion were inhibited completely by L-NAME pretreatment and partially by 1H-[1,2,4]oxadiazol

66 In a drug-free test on Day 8, copulation by L-NAME-treated rats was similar to that of unexposed con

67 d the increased migration to IL-8 induced by L-NAME.

68 he sustained, severe hypertension induced by L-NAME.

69 This was inhibitable by L-NAME (NO synthase inhibitor), wortmannin (phosphatidyl

70 scue of tube formation in GSNOR(-/-) MSCs by L-NAME or the GHRH agonists JI-38, MR-409, and MR-356.

71 hese data indicate that inhibition of NOS by L-NAME results in a significant (19 %) speeding of pulmo

72 These effects were prevented by L-NAME.

73 in RBF and the consequent increase in RVR by L-NAME with a potency order of CYP4A2 = CYP4A1 > CYP4A3.

74 Inhibition of nitric oxide (NO) synthase (by L-NAME; N(G)-nitro-L-arginine methyl ester) and blockade

75 ine; these responses were also unaffected by L-NAME.

76 In vivo A-779 or combined L-NAME and nimesulide treatment corrects it.

77 In contrast, L-NAME treatment further decreased HAP which impaired he

78 In contrast, L-NAME virtually abolished the change in permeability (d

79 steady state exercise over 5 min (control), L-NAME was infused for 5 min, followed by 2 min saline,

80 During L-NAME treatment, the absence of renal ACE was associate

81 led the pattern in reference subjects during L-NAME administration and was minimally affected by L-NA

82 ith N(omega)-nitro-L-arginine methyl ester ( L-NAME) abolished the inhibitory effect of gAd on leukoc

83 Nomega-L-nitromethyl arginine ester (L-NAME, 25 mg kg(-1)), an inhibitor of NO production, in

84 without N(G)-nitro-L-arginine methyl ester (L-NAME) (100 micromol/L), or 5-hydroxydecanoate (100 mic

85 OS) with N(G)-nitro-L-arginine methyl ester (L-NAME) accelerates the 'phase II' pulmonary O2 uptake (

86 nduced by l-N(G)-nitroarginine methyl ester (L-NAME) and pressure overload (n=11) from transaortic co

87 hase with L-N(G)-nitroarginine methyl ester (L-NAME) and stimulation of growth hormone-releasing horm

88 bitor L-N(omega)-Nitroarginine methyl ester (L-NAME) and the anti-oxidant N-acetylcysteine (NAC).

89 nhibitor N(w)-nitro-L-arginine methyl ester (L-NAME) before aerosol challenge with Ascaris suum, and

90 s with Nomega-nitro-L-arginine methyl ester (L-NAME) blocked the increase in RBF.

91 NG-nitro-L-arginine methyl ester (L-NAME) constricted and indomethacin dilated the arterie

92 inhibitor NG-nitro-l-arginine methyl ester (L-NAME) for 14 days plus Ang II during days 8 through 14

93 ibitor Nomega-nitro-L-arginine methyl ester (L-NAME) for 30 minutes, followed by the addition of SPR.

94 usion of N(G)-nitro-L-arginine methyl ester (L-NAME) for 5 min to inhibit NOS during continuous SS hy

95 inhibitor L-N(G)-nitroarginine methyl ester (L-NAME) from gestational day (GD) 11 to GD18 to induce h

96 nhibitor N(6)-nitro-L-arginine methyl ester (L-NAME) in drinking water (NLN, IHLN and CHLN regimes) t

97 o using the L-NG-Nitroarginine Methyl Ester (L-NAME) induced PE-like rat models, also characterized b

98 2 mM N(omega)-nitro-L-arginine methyl ester (L-NAME) or 50 microM Reactive blue-2 (RB2) beginning 30

99 inhibitor NW-nitro-L-arginine methyl ester (L-NAME) or its inactive isomer NW-nitro-D-arginine methy

100 idomine or NG-nitro-L-arginine methyl ester (L-NAME) or saline were applied daily.

101 inhibitor NG-nitro-L-arginine methyl ester (L-NAME) or the ATP-sensitive mitochondrial potassium cha

102 e that L-N(G)-nitro-L-arginine methyl ester (L-NAME) pretreatment blocked, whereas L-arginine and sod

103 nhibitor N(G)-nitro-l-arginine methyl ester (L-NAME) significantly (P < 0.001) enhanced IL-8-induced

104 e probe and N-nitro-L-arginine methyl ester (L-NAME) through the second.

105 ose or Nomega-nitro-l-arginine methyl ester (L-NAME) treatment.

106 ine or Nomega-nitro-L-arginine methyl ester (L-NAME) was administered to stimulate or block NO synthe

107 ition by N(G)-nitro-L-arginine methyl ester (L-NAME) was much greater in LPS-treated mice (41 versus

108 hase (NOS) by nitro-L-arginine methyl ester (L-NAME) would alleviate the inhibition of mitochondrial

109 Keto), (2) NG-nitro-l-arginine methyl ester (L-NAME), (3) Keto + l-NAME (Combo), and (4) Ringer solut

110 xercise (N(G)-nitro-L-arginine methyl ester (L-NAME), 25 mg over 5 min to inhibit NO synthase (NOS);

111 hibited using l-nitro arginine methyl ester (L-NAME), a competitive inhibitor of NOS.

112 resence of NG-nitro-L-arginine methyl ester (L-NAME), a general inhibitor of NO synthesis.

113 nses; N-omega-nitro-l-arginine methyl ester (L-NAME), a nonselective nitric-oxide synthase (NOS) inhi

114 N(G)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synthase, exacerbated monocr

115 N-nitro-l-arginine methyl ester (L-NAME), an NO synthase inhibitor, also decreased urine

116 L-NG-nitroarginine methyl ester (L-NAME), but not D-NG-nitroarginine methyl ester, increa

117 ed by L-N(omega)-nitroarginine methyl ester (L-NAME), indicating uncoupling of eNOS activity.

118 nhibitor N(G)-nitro-L-arginine methyl ester (L-NAME), or by bilateral vagotomy.

119 saline, N(G)-L-nitro-arginine methyl ester (L-NAME), or N-acetylcysteine for 7 days from week 3 to w

120 hibitor, N(G)-nitro-l-arginine methyl ester (L-NAME), potentiated LT release in a dose-dependent mann

121 bitor, Nomega-nitro-L-arginine-methyl ester (L-NAME), significantly inhibited Ox-PAPC-induced IL-8 sy

122 nhibitor N(G)-nitro-L-arginine methyl ester (L-NAME), the guanylyl cyclase inhibitor 1H- [1,2,4]oxadi

123 t of VEC with nitro-L-arginine methyl ester (L-NAME), while inhibiting the release of nitrate, does n

124 wild-type, N-nitro-L-arginine methyl ester (L-NAME)-treated (with 1 mg/mL in drinking water), and eN

125 les from N(G)-nitro-L-arginine methyl ester (L-NAME)-treated male and ovariectomized female rats befo

126 nhibitor N(G)-nitro-L-arginine methyl ester (L-NAME).

127 opine or N(G)-nitro-l-arginine methyl ester (L-NAME).

128 reated with N-nitro-L-arginine methyl ester (L-NAME).

129 nhibitor N(G)-nitro-l-arginine methyl ester (L-NAME).

130 inhibitor NG-nitro-L-arginine methyl ester (L-NAME).

131 ent with L-N(G)-nitro arginine methyl ester (L-NAME).

132 bitor, Nomega-Nitro-L-arginine methyl ester (L-NAME).

133 inhibitor l-N(G)-nitroarginine methyl ester (L-NAME).

134 bitor [Nomega-nitro-L-arginine methyl ester (L-NAME)], or scavenging NO with a ruthenium-based scaven

135 NOS with N(G)-nitro-L-arginine methyl ester (L-NAME, 1 mM).

136 ibitor of NOS, L-nitroarginine methyl ester (L-NAME, 200 microM), significantly decreased the swimmin

137 nhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg/day) on energy intake, bodyweight and h

138 P-2 plus N(G)-Nitro-L-arginine methyl ester (L-NAME, 50 micromol x kg(-1) x hour(-1)) for 4 hours eac

139 nions) or L-N(G)-nitroarginine methyl ester (L-NAME, a nonselective nitric oxide synthase inhibitor)

140 oinjection of L-nitro-arginine methyl ester (L-NAME, an NO synthesis inhibitor) into the MPOA blocked

141 hibitor, N(G)-nitro-L-arginine methyl ester (L-NAME; 10 mg/kg per day in drinking water).

142 ase with N(G)-nitro-L-arginine methyl ester (L-NAME; 300 microm) eliminated this ACh- or flow-induced

143 A or N(omega)-nitro-L-arginine methyl ester (L-NAME; each 250 micromol x kg(-1) x d(-1)) by use of os

144 N omega-Nitro-L-arginine-methyl-ester (L-NAME) augmented the myogenic response similarly in all

145 Nomega-nitro-L-arginine-methyl-ester (L-NAME) or placebo was administered to 22 and 15 wild-ty

146 synthesis (L-NG-nitroarginine methyl ester [L-NAME]) or protein nitrosylation (via dithiothreitol) o

147 ion (N(omega)-nitro-l-arginine methyl ester [L-NAME]).

148 n (10 mM N(G)-nitro-L-arginine methyl ester, L-NAME); low-dose NO infusion (1.0 microM sodium nitropr

149 on of L-Nomega-nitro-arginine methyl esther (L-NAME), an inhibitor of nitric oxide synthase, before u

150 After achieving steady-state exercise, L-NAME (25 mg) was infused over 5 min to inhibit NO synt

151 response was significantly smaller following L-NAME infusion (22.1 +/- 2.4 vs. 17.9 +/- 2.3; P < 0.05

152 periostin expression protected animals from L-NAME-induced renal injury.

153 Only microparticles from L-NAME and not untreated or D-NAME-treated neutrophils i

154 st of PAI-1, were effectively protected from L-NAME-induced thrombosis.

155 Rats placed on cholate-rich diets and given L-NAME had increased intrahepatic and biliary levels of

156 Group 2 (n = 10) was given L-NAME (100 microL, 10 mg/mL) followed by NP (50 microL,

157 In cultured hepatocytes, L-NAME or dithiothreitol blocked cholate-induced down-re

158 Nitro-L-arginine methyl ester hydrochloride (L-NAME) afforded partial protection.

159 Nitro-L-arginine methyl ester hydrochloride (L-NAME) infusion.

160 nitro-L-arginine methyl ester hydrochloride (L-NAME) or NG-monomethyl-L-arginine (L-NMMA) reduced the

161 nitro-L-arginine methyl ester hydrochloride (L-NAME), including the reversal of the caveolin-1-null m

162 nitro-L-arginine methyl ester hydrochloride (L-NAME)/high salt or repeated angiotensin II stimulation

163 Compared with saline-drinking mice, Ang II/L-NAME-treated mice had significantly increased heart to

164 Ang II/L-NAME-treated mice showed glomerular ischemia, proteinu

165 The response was also absent in L-NAME plus low-dose SNP sites and not altered by low-do

166 nt of tachyphylaxis to PBG in saline- and in L-NAME-treated rats whereas the BJR responses elicited b

167 In contrast, CBF in L-NAME-treated fetuses increased to only 115 % of the re

168 e factor 1alpha immunostaining was higher in L-NAME vs control mice at GD14.

169 MECVF was higher in L-NAME-treated animals (0.43+/-0.09 versus 0.26+/-0.03,

170 K(Ca)2.3 activity was lost in L-NAME-treated arteries, but was restored by Rho kinase

171 aseline in each group) but was much lower in L-NAME-treated and eNOS-/- mice (17.4+/-1.6 and 20.4+/-1

172 he CVC response to whole-body heat stress in L-NAME sites was significantly reduced (32 +/- 3% CVC(ma

173 NO, PNO), reduced by NO synthase inhibition (L-NAME groups: CL-Name, PL-Name), or not manipulated (gr

174 After NO synthase inhibition (L-NAME), thrombin contracted aged arteries, which was in

175 trite scavenger Urate, or the eNOS inhibitor L-NAME and these effects as well as eNOS activation were

176 of PR39-induced mice with the eNOS inhibitor L-NAME in the last 3 weeks of a 6-week stimulation perio

177 uced by XMJ were abolished by eNOS inhibitor L-NAME or specific eNOS siRNA in H2O2-treated cells.

178 ther the Src inhibitor PP2 or eNOS inhibitor L-NAME.

179 stic and performance effects of NO inhibitor L-NAME and cGMP inhibitor LY-83583.

180 amnestic effects of pretraining NO inhibitor L-NAME.

181 thase (eNOS) with the specific NOS inhibitor L-NAME (N(G)-nitro-l-arginine methyl ester) led to incre

182 NOS inhibitor L-NAME also significantly attenuated RGS4 degradation, a

183 The NOS inhibitor L-NAME normalized pressure-dependent drainage in transge

184 imulation, is prevented by the NOS inhibitor L-NAME or in nNOS-deleted mice.

185 us treatment of cells with the NOS inhibitor L-NAME resulted in telomere elongation and prevention of

186 by the nitric-oxide synthase (NOS) inhibitor L-NAME (N(D)-nitro-L-arginine methyl ester).

187 of the nitric oxide synthase (NOS) inhibitor L-NAME and in mice with neuronal and inducible NOS defic

188 Nitric oxide (NO) synthase inhibitor L-NAME nearly abolished dilations to bradykinin and flow

189 cell cultures with the NO synthase inhibitor L-NAME or the NO scavenger hemoglobin increased cell pro

190 The NO synthesis inhibitor L-NAME increased ABP, decreased HR and greatly reduced F

191 ase inhibitors, but not by the NO inhibitor, L-NAME.

192 oxide synthase with a nonspecific inhibitor, L-NAME, had no effect on luminol-mediated chemiluminesce

193 .v.) in rats treated with the NOS inhibitor, L-NAME (25 micromol/kg, i.v.) elicited similar reduction

194 ed treatment with the NO synthase inhibitor, L-NAME, and the NO donor, sodium nitroprusside.

195 o NOS and guanylate cyclase (GC) inhibitors (L-NAME, ODQ), which induced aging and relatively resista

196 ls were elevated in tumors receiving post-IR L-NAME.

197 beta (Abeta) (control 10.93 +/- 0.70 pg/mL; L-NAME 168.21 +/- 27.38 pg/mL; P<0.001).

198 e 4 received substance P combined with 10 mm L-NAME plus 500 microm pyrilamine.

199 te 2 received a continuous infusion of 10 mM L-NAME to inhibit NO synthase.

200 e 2 received substance P combined with 10 mm L-NAME to inhibit NO synthase.

201 inger solution), NOS inhibited (NOS-I, 10 mM L-NAME), A-I (5 mM BEC + 5 mM nor-NOHA), L-arg supplemen

202 crom dose of substance P combined with 10 mM L-NAME.

203 een 8 and 45 mm Hg, using mock AH +/-100 muM L-NAME.

204 Neither L-NAME nor inhaled NO altered lung permeability in the s

205 an inhibitor of nitric oxide synthase (NOS), L-NAME, blocked signaling.

206 myocytes, HOE 642 and streptomycin, but not L-NAME, ablated the stretch-induced increase in [Ca(2+)]

207 The ability of L-NAME-induced microparticles to enhance migration was f

208 h were infused in the presence or absence of L-NAME in similar subjects.

209 Addition of L-NAME reduced FBF to 83 +/- 3% of control, and it remai

210 Administration of L-NAME before pGz completely reversed this protection, w

211 hosis, and decreased after administration of L-NAME but were unchanged by N-acetylcysteine.

212 Intraperitoneal administration of L-NAME decreased hypothalamic NO content in both chow-fe

213 After administration of L-NAME, CBF decreased by 14 +/- 6 % (P < 0.01) despite i

214 hich was abated by post-IR administration of L-NAME.

215 Attenuation of L-NAME-inhibitable superoxide anion levels by GW501516 d

216 Coadministration of L-NAME and iberiotoxin almost abolished the vasodilation

217 he presence of L-NAME and the combination of L-NAME plus pyrilamine.

218 g rats chronically with a subpressor dose of L-NAME beginning 2 d before nephrectomy blocked the incr

219 although other mechanisms for the effect of L-NAME on .VO2 kinetics remain to be explored.

220 We examined the effect of L-NAME, an inhibitor of NO synthase, on CSD-induced tole

221 imum, 15% +/- 2%; n = 33), with no effect of L-NAME.

222 ption by Ox-PAPC, we examined the effects of L-NAME on Ox-PAPC-induced SREBP activation.

223 nt study was to investigate the influence of L-NAME on pulmonary VO2 kinetics following the onset of

224 max, preceded either by systemic infusion of L-NAME (4 mg kg(-1) in 50 ml saline) or 50 ml saline as

225 th and without prior intravenous infusion of L-NAME (4 mg kg-1 in 50 ml saline over 60 min).

226 trol conditions (27 +/- 4%), and infusion of L-NAME during continuous SS hypoxia reduced FVC by -36 +

227 The infusion of L-NAME elicited a 35 +/- 4% decrease in CVC at the L-NAM

228 Infusion of L-NAME with physiological saline led to a significant de

229 and B. Woodside report that the injection of L-NAME into the 3rd ventricle, which would suppress the

230 ture research utilizing direct injections of L-NAME into specific neural sites is needed to resolve t

231 In the presence of L-NAME and indomethacin, dilation to 10(-4) M ATP was si

232 significantly attenuated in the presence of L-NAME and the combination of L-NAME plus pyrilamine.

233 In the presence of L-NAME, the addition of SNAP (1 microM) produced modest

234 er acute intracerebroventricular (i.c.v.) of L-NAME was also measured.

235 er the administration of N-acetylcysteine or L-NAME.

236 earts from wild-type mice than in eNOS-/- or L-NAME-treated hearts.

237 and RVR responses to angiotensin II, NE, or L-NAME were similar in both groups.

238 y corrected by in vivo A-779, nimesulide, or L-NAME.

239 ultiple topical treatments of 500 mug SNP or L-NAME to one eye.

240 Animals received either vehicle or L-NAME (4 mg/kg, iv) 30 min before CSD.

241 Co-infusion of GLP-2 plus L-NAME did not increase either PDV blood flow rate or gl

242 anterograde amnestic effects of pretraining L-NAME.

243 In other naive rats, L-NAME or saline was microinjected into the MPOA before

244 vascular nitrite reductase activity, in RBCs L-NAME, L-NMMA, and L-arginine inhibited nitrite-derived

245 echanism in cultured Jurkat T cells revealed L-NAME suppression of IR-induced IL10 expression, which

246 Saline, L-NAME (20 mM; to inhibit NOS activity) and sodium nitro

247 hibitors of inducible nitric oxide synthase (L-NAME and NCX-4016).

248 elective inhibitor of nitric oxide synthesis L-NAME (L-nitro-arginine methyl ester), which had no eff

249 The results showed that L-NAME and LY-83583 produced significant anterograde and

250 erence between the L-NAME-only sites and the L-NAME plus pyrilamine sites.

251 elicited a 35 +/- 4% decrease in CVC at the L-NAME and BT + L-NAME sites (P < 0.05); subsequent slow

252 % of initial baseline decrease in CVC at the L-NAME treated sites (P < 0.05).

253 re was no significant difference between the L-NAME-only sites and the L-NAME plus pyrilamine sites.

254 moxifen exhibits antifibrotic effects in the L-NAME model of hypertensive nephrosclerosis, likely thr

255 to a higher temperature in 4 subjects in the L-NAME sites (control, 37.0 +/- 0.3 degrees C, n = 16; L

256 hyphylaxis to PBG was markedly faster in the L-NAME-treated rats.

257 In the L-NAME/high-salt model, memory T cells of the kidney wer

258 In addition to L-NAME, the guanylyl cyclase inhibitors ODQ and thrombos

259 prolonged heating, which was insensitive to L-NAME in low-flow POTS subjects.

260 ols, whereas by 14 and 28 d, the response to L-NAME was similar to controls.

261 els, and enhanced natriuresis in response to L-NAME.

262 temic and renal vasoconstrictor responses to L-NAME were also similar in all genotypes.

263 ontrol mice displayed similar sensitivity to L-NAME in older oocytes, although to a significantly low

264 induced by radiation in a manner similar to L-NAME.

265 Topical L-NAME had no effect on IOP, PD, Rfx, or MAP.

266 ll apoptosis, which could be inhibited using L-NAME.

267 -term nitric oxide synthase inhibition using L-NAME.

268 d EVP to 13.9 +/- 1.7 mm Hg (P < 0.01 versus L-NAME and baseline).

269 20.7 +/- 1.3 mm Hg after NP (P < 0.01 versus L-NAME and P > 0.05 versus baseline).

270 reater with L-NAME (Con: 14.0 +/- 2.1 versus L-NAME: 16.0 +/- 1.6 s; P = 0.03), suggestive of a slowe

271 reduced with L-NAME (Con: 4.0 +/- 1.1 versus L-NAME: 2.7 +/- 2.1 mM; P = 0.04).

272 y 44% with L-NAME (Con: 36.3 +/- 17.3 versus L-NAME: 20.4 +/- 8.3 s; P = 0.01).

273 completely reversed this protection, whereas L-NAME alone did not affect the antigen-induced response

274 II VO2 time constant was reduced by 44% with L-NAME (Con: 36.3 +/- 17.3 versus L-NAME: 20.4 +/- 8.3 s

275 is attenuated by NO synthesis blockade with L-NAME, but restored when baseline FVC is restored by in

276 es pretreated with substance P combined with L-NAME (20 +/- 2% CVC(max)) and was significantly reduce

277 es pretreated with substance P combined with L-NAME (27 +/- 2% CVC(max); P < 0.001).

278 g times in BKB2R(-/-) mice also correct with L-NAME and nimesulide therapy.

279 The duration of 'phase I' was greater with L-NAME (Con: 14.0 +/- 2.1 versus L-NAME: 16.0 +/- 1.6 s;

280 rebral GLUT1 immunoreactivity increased with L-NAME, with or without hypoxia, especially in CHLN rats

281 el of nitric oxide synthesis inhibition with L-NAME.

282 bserved during treatment of MyMRKO mice with L-NAME/Ang II.

283 Blockade of NO synthase (NOS) with L-NAME increased baseline FVR and facilitated the sympat

284 e significantly reduced by pretreatment with L-NAME.

285 actate during exercise was also reduced with L-NAME (Con: 4.0 +/- 1.1 versus L-NAME: 2.7 +/- 2.1 mM;

286 results with D-AP5 and current results with L-NAME and LY-83583 together suggest that the NMDA recep

287 th LY294002 (10 microm) nor NO synthase with L-NAME (1 mm) reduced the slow force response in muscle

288 inhibiting nitric oxide (NO) synthesis with L-NAME (N(omega)-nitro-L-arginine methyl ester hydrochlo

289 Acute inhibition of NO synthesis with L-NAME in uninephrectomized rats caused a greater decrea

290 ic inhibition of nitric oxide synthesis with L-NAME).

291 ell volumes were higher in mice treated with L-NAME compared with controls (P<0.001).

292 xtent in induced EC-Akt Tg mice treated with L-NAME, suggesting that some of the vascular protective

293 Treatment with L-NAME (NG-mono-methyl-L-arginine ester) or nimesulide s

294 In contrast to treatment with L-NAME alone, combined fetal treatment with L-NAME and n

295 and 17 +/- 1 pg/microg after treatment with L-NAME and N-acetylcysteine, respectively (P < .05).

296 L-NAME alone, combined fetal treatment with L-NAME and nitroprusside prevents generalized vasoconstr

297 Treatment with L-NAME increased systemic arterial mean pressure (SAP; 1

298 Treatment with L-NAME or TEMPOL protected retinal neurons and confirmed

299 d flow that was suppressed by treatment with L-NAME, an eNOS inhibitor.

300 rterial pressure in SHR rats, but not in WKY/L-NAME rats.