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1 ith a nonselective inhibitor (Nomega-nitro-L-arginine methyl ester).
2 ynthase (NOS) inhibitor L-NAME (N(D)-nitro-L-arginine methyl ester).
3 d absence of the eNOS inhibitor N(G)-nitro-L-arginine methyl ester.
4 oxide synthase (eNOS) inhibitor N(G)-nitro-L-arginine methyl ester.
5 d by using a specific NOS inhibitor, nitro-l-arginine methyl ester.
6  synthesis was inhibited by N(omega)-nitro-l-arginine methyl ester.
7 ular L-arginine and was inhibited by L-nitro-arginine methyl ester.
8  was not significantly affected by N-nitro-L-arginine methyl ester.
9 ar endothelium with 50 micromol/L NG-nitro-L-arginine methyl ester.
10 y altered in response to glucose and L-nitro-arginine methyl ester.
11 t was abrogated by administration of nitro-l-arginine methyl ester.
12  was reduced by tetrodotoxin or N(G)-nitro-l-arginine methyl ester.
13 nitric oxide synthase with N(omega) -nitro-l-arginine methyl ester.
14 e nitric oxide synthase inhibitor NG-nitro-l-arginine methyl ester.
15 nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester.
16 henyltheophylline in the presence of L-nitro-arginine-methyl ester.
17 cts inhibited by the NOS inhibitor N-nitro-L-arginine-methyl ester.
18 in) followed by a 10-min infusion of L-nitro-arginine-methyl ester (0.5 mg/kg x min).
19 1) for 28 days) or treatment with NG-nitro-L-arginine methyl ester (1 mg/mL in drinking water for 28
20 whereas its inactive enantiomer N(w)-nitro-D-arginine methyl ester (1 mM) resulted in microglial accu
21 pplication of the NOS inhibitor N(w)-nitro-L-arginine methyl ester (1 mM) significantly reduced micro
22 er inhibition of NO synthase with NG-nitro-L-arginine methyl ester (1 to 2 mg/kg IV) had raised the p
23  nitric oxide synthase inhibitors Ng-nitro-L-arginine-methyl ester (1.5 mmol/L) and aminoguanidine (1
24                               Nomega-Nitro-L-arginine methyl ester 10(-4) mol/L modestly impaired FID
25 transcription inhibitor; or N(omega)-nitro-L-arginine methyl ester (10(-4) mol/L), an inhibitor of NO
26 ed after NO synthase blockade with N-nitro-L-arginine methyl ester (10(-4) mol/L; all P<0.05).
27                                 N(G)-nitro-l-arginine methyl ester (100 mumol/L) or a protease-activa
28 tive NO* synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (100-800 nmol) as well as by the s
29                                      L-Nitro-arginine methyl ester (15 mg kg(-1)), an inhibitor of en
30  blockade of NO production with N(G)-nitro-L-arginine-methyl ester (2 micromol; delivered ICV, 30 min
31          The NO synthase inhibitor N-nitro-L-arginine methyl ester (200 microM) reversed this oxidant
32  events were blocked by L-NAME (N(G)-nitro-L-arginine methyl ester, 3-30 mg/kg), a nitric oxide synth
33 nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (30 mg/kg iv) was administered.
34 s blocked by the NOS inhibitors N(G)-nitro-L-arginine methyl ester (30 microm) or N(G)-monomethyl-L-a
35 nonselective NOS inhibitor (N(omega)-nitro-L-arginine methyl ester; 30 mg/kg), a soluble guanylyl cyc
36 ic oxide synthase inhibitor (N-omega-nitro-L-arginine methyl ester, 50 mg/kg/day) or peroxynitrite sc
37  synthase (NOS) inhibition with N(W)-nitro-L-arginine methyl ester (60 mg/kg), vasoconstriction induc
38           Moreover, l-NAME (N(omega)-nitro-l-arginine-methyl ester), a specific inhibitor of nitric o
39                               Nomega-nitro-L-arginine methyl ester, a nonspecific inhibitor of endoge
40 stically amplified by co-addition of tosyl-l-arginine methyl ester, a small molecule that blocks the
41                             N(omega)-nitro-l-arginine methyl ester abolished the systemic but not the
42  rings, which was unaffected by L(G)-nitro-l-arginine methyl ester addition and inhibited by the guan
43 creased significantly more than with L-nitro-arginine-methyl ester alone, but there were no further i
44  The inhibition of eNOS with N-omega-nitro-L-arginine methyl ester also potently reduced retinal leuk
45 eatment with the eNOS inhibitor N(G)-nitro-L-arginine methyl ester also reduced endothelial cell migr
46 s 7-nitroindazole (7-NI) and N-omega-nitro-L-arginine methyl ester also reduced NMDA toxicity.
47 antly inhibited in the presence of N-nitro-L-arginine methyl ester (an inhibitor of NOS) and wortmann
48 kinase (ERK) inhibitor, and N(omega)-nitro-L-arginine methyl ester, an antagonist of nitric oxide syn
49 he effects of nicardipine; N omega-I-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synt
50 ebroventricular infusion of N(omega)-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synt
51 a)) channels, respectively, and N(G)-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synt
52 horylation, which was abolished by N-nitro-L-arginine methyl ester, an inhibitor of nitric oxide synt
53 nthase expression; in contrast, N(G)-nitro-L-arginine methyl ester, an inhibitor of NO synthase, inhi
54       Pretreatment of rats with L-N(G)-nitro arginine methyl ester, an inhibitor of NO synthase, prev
55 f NFkappaB into the nucleus, 3) N(G)-nitro-l-arginine methyl ester, an inhibitor of NO synthesis, abo
56             The administration of NG-nitro-L-arginine methyl ester, an inhibitor of NOS activity, inc
57 expression was abrogated by N(omega)-nitro-l-arginine methyl ester, an inhibitor of NOS.
58                             N(omega)-Nitro-L-arginine methyl ester and 1H-[1,2,4]-oxadiazolo-[4,3-a]-
59 learance, whereas infusion of Nomega-nitro-L-arginine methyl ester and a high dose of aminoguanidine
60 e, because it was not inhibited by N-nitro-l-arginine methyl ester and also occurred in vascular smoo
61 presence of the NOS inhibitors, N(G)-nitro-L-arginine methyl ester and aminoguanidine; in addition, t
62               The NOS inhibitor N(G)-nitro-l-arginine methyl ester and genistein, wortmannin, or NF-k
63 ic mice during coadministration of N-nitro-l-arginine methyl ester and indomethacin.
64 acid and by NO synthase inhibitor NG-nitro-L-arginine methyl ester and NG-monomethyl-L-arginine.
65 nd inhibition of NO synthase by N(G)-nitro-L-arginine methyl ester and of soluble guanylyl cyclase by
66 nd NOS1-specific NOS inhibitors N(G)-nitro-l-arginine methyl ester and S-methyl-l-thiocitrulline, res
67 ic oxide synthase inhibitors N-omega-nitro-L-arginine methyl ester and S-methyl-thiocitrulline.
68 r treatment with a combination of NG-nitro-l-arginine methyl ester and sodium nitroprusside.
69 treatment with a combination of N(G)-nitro-L-arginine methyl ester and sodium nitroprusside.
70 nitric oxide synthase inhibitor N(G)-nitro-l-arginine methyl ester and the neuronal blocker tetrodoto
71 ith the nonspecific NOS inhibitor NG-nitro-L-arginine methyl ester and the NOS1-specific inhibitor 7-
72 on by the NO synthase inhibitor N(G)-nitro-l-arginine methyl ester and the superoxide dismutase mimic
73 stitutive NO synthase inhibitor N(G)-nitro-l-arginine methyl ester and unresponsive to stimulation by
74 of NKCC1, whereas the antioxidants N-nitro-l-arginine methyl ester and uric acid all significantly di
75 bility, and pretreatment with both N-nitro-L-arginine methyl ester and wortmannin inhibited the Tat-i
76                     In RAW cells, Ng-nitro-L-arginine-methyl ester and AG block IFNgamma/LPS-activate
77 oxide (NO) synthase (by L-NAME; N(G)-nitro-L-arginine methyl ester) and blockade of soluble guanylyl
78 iated arginine and singly hydrated lithiated arginine methyl ester are different and contain spectral
79 d arginine, sodiated arginine, and lithiated arginine methyl ester are investigated using infrared ac
80 d alkali metal cationized arginine (Arg) and arginine methyl ester (ArgOMe) are investigated with inf
81                   NOS inhibitor N(G)-nitro-L-arginine methyl ester attenuated the endothelial barrier
82                 The NOS inhibitor, N-nitro-L-arginine methyl ester, attenuated the microvascular leak
83 ac1 inhibitor NSC 23766 but not an N-nitro-L-arginine-methyl ester-attenuated ESR O2*- signal at 30 m
84 tion of nitric oxide synthase with N-nitro-L-arginine methyl ester, but not with the inactive D-isome
85 se appeared to be unaffected by N(G)-nitro-L-arginine methyl ester, but the second rise was reduced.
86              In the presence of K(G)-nitro-L-arginine methyl ester, ceramide produced no further inhi
87 tric oxide synthase inhibitor Nomega-nitro-L-arginine methyl ester completely abrogated the increase
88 letely by superoxide dismutase and N-nitro-L-arginine methyl ester, consistent with the hypothesis th
89 ive effect of the NOS inhibitor N(G)-nitro-L-arginine methyl ester could be attributed to dramaticall
90 r the glycine (CyGly), arginine (CyArg), and arginine methyl ester (CyArgOMe) derivatives.
91 r (L-NAME) or its inactive isomer NW-nitro-D-arginine methyl ester (D-NAME) and were trained on a neg
92 hyl ester (L-NAME; 8 mg/kg), or N(G)-nitro-D-arginine methyl ester (D-NAME; 8 mg/kg).
93                The NOS inhibitors, N-nitro-L-arginine methyl ester, dexamethasone and indomethacin po
94 nd inhibition of NOS activity with N-nitro-L-arginine methyl ester did not block the beneficial effec
95 nitric oxide synthesis inhibitor, NG-nitro-l-arginine methyl ester, did not reverse the inhibitory ef
96 e non-isoform-specific NOS inhibitor L-nitro-arginine methyl ester during 3 weeks of remobilization h
97 ion of nitric oxide synthase by N(w)-nitro-L-arginine methyl ester eliminated antiadrenergic effects
98           Group 2 similarly received L-nitro-arginine-methyl ester followed by 8-sulfophenyltheophyll
99 Aromatic templates also transported N-acetyl arginine methyl ester from water to 1-octanol.
100 e vascular bed of the cat, N omega-I-nitro-L-arginine methyl ester, glibenclamide, and meclofenamate
101 xin or BAPTA-AM, but not by N(omega)-nitro-L-arginine methyl ester, glipizide, indomethacin or 17-oct
102 more, the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester had no effect on sperm-induced Ca(
103 ated with ceramide, whereas N(omega)-nitro-l-arginine methyl ester had no effect.
104 oxide (NO) synthase inhibitors N(G)-nitric-L-arginine methyl ester HCl (L-NAME) or N(G)-nitro-L-argin
105 d with NO synthase inhibitors (N(G)-Nitric-L-arginine methyl ester HCl (L-NAME), N(G)-Nitro-L-arginin
106 with the NO synthase inhibitor N(G)-nitric-L-arginine methyl ester HCl (L-NAME), the NO donors were s
107 were quantified in wild-type, Nomega-nitro-L-arginine methyl ester HCl salt (L-NAME)-treated, nNOS(-/
108                             N(omega)-Nitro-L-arginine methyl ester, HOE-140, and dichloroisocoumarin
109 tric oxide synthase inhibitor Nomega-Nitro-L-arginine methyl ester hydrochloride (L-NAME) afforded pa
110 iting NO synthase activity with N(G)-nitro-L-arginine methyl ester hydrochloride (L-NAME) blocked TG-
111 ercentage decrease in response to NG-Nitro-L-arginine methyl ester hydrochloride (L-NAME) infusion.
112 oronary VEGF165 0.25 microg/kg/min + nitro-L-arginine methyl ester hydrochloride (L-NAME) or 5) rapid
113 s with the NO synthase inhibitors NG-nitro-L-arginine methyl ester hydrochloride (L-NAME) or NG-monom
114 he broad-spectrum NOS inhibitor N(g)-nitro-L-arginine methyl ester hydrochloride (L-NAME) via their d
115 dministration of the NOS inhibitor N-nitro-L-arginine methyl ester hydrochloride (L-NAME), including
116 ive challenges using either N(omega)-nitro-L-arginine methyl ester hydrochloride (L-NAME)/high salt o
117 Ringer's (control); (2) 20 mm Nomega-nitro-l-arginine methyl ester hydrochloride (non-selective NOS i
118  1400W had no effect, whereas Nomega-nitro-l-arginine methyl ester hydrochloride caused a partial red
119                 Incubation of Nomega-nitro-l-arginine methyl ester hydrochloride or 1400W (a nonselec
120 tric oxide synthesis antagonist N(G)-nitro-L-arginine methyl ester hydrochloride or by hemoglobin but
121 production, which was inhibited by N-nitro-l-arginine methyl ester hydrochloride, indicating uncoupli
122 of DTT and the NO inhibitor N(omega)-nitro-L-arginine methyl ester hydrochloride, the ability of CO t
123 (NO) synthesis with L-NAME (N(omega)-nitro-L-arginine methyl ester hydrochloride; 5 mg/kg; i.v.).
124 nd U(cGMP) were suppressed by Nomega-nitro-L-arginine methyl ester in SOD-Tg-db/db but not in NTg-db/
125 th the competitive NOS inhibitor, NG-nitro-l-arginine methyl ester, in cells grown in l-arginine rest
126 form of nitric oxide synthase with N-nitro-L-arginine methyl ester increased DOX-induced mortality.
127 hydro-6-methyl-4H-1,3-thiazine and N-nitro-L-arginine methyl ester) increased RSV titers in the lungs
128 ereas the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester increases ceramide-induced vWF rel
129  vascular resistances increased with L-nitro-arginine-methyl ester infusions, and 8-sulfophenyltheoph
130 availability and reduced basal and N-nitro-l-arginine methyl ester-inhibitable O(2)(.-) in internal m
131 d eNOS uncoupling, as assessed by NG-nitro-l-arginine methyl ester-inhibitable superoxide production,
132 sociated with reduced total and N(G)-nitro-L-arginine methyl ester-inhibitable superoxide, suggesting
133                                 N(w)-nitro-L-arginine methyl ester, inhibitor of NO synthase, attenua
134                                 N(G)-nitro-L-arginine methyl ester inhibits the effect of isoproteren
135 ally, blockade of eNOS with N(omega)-nitro-L-arginine methyl ester ( L-NAME) abolished the inhibitory
136 ase material to examine the feasibility of L-Arginine methyl ester (L-AME) functionalized material fo
137 attenuated after NOS blockade with N-nitro-L-arginine methyl ester (L-NAME) (-2+/-5%, -3+/-2%, and -6
138     Addition of the NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME) (1 mg/ml) to the drinking
139           Pretreatment with N(omega)-nitro-l-arginine methyl ester (l-NAME) (10(-3) mol/L), propranol
140  (1 micromol/L) with or without N(G)-nitro-L-arginine methyl ester (L-NAME) (100 micromol/L), or 5-hy
141 as unaffected by 100 microM N(omega)-nitro-L-arginine methyl ester (L-NAME) (68 +/- 4 vs. 66 +/- 3% i
142 ; 4) L-arginine before IR; and 5) Nw-Nitro-L-arginine methyl ester (L-NAME) + IPC before IR.
143 itric oxide synthase (NOS) with N(G)-nitro-L-arginine methyl ester (L-NAME) accelerates the 'phase II
144               The NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) administered after blast
145 nd mechanism of action of Mb on N(G)-Nitro-L-arginine Methyl Ester (L-NAME) and Deoxycorticosterone A
146 m baseline, nine animals received NG-nitro-L-arginine methyl ester (L-NAME) at 15 mg/kg to restore MA
147 nitric oxide synthase inhibitor N(w)-nitro-L-arginine methyl ester (L-NAME) before aerosol challenge
148 hibition of NO synthesis with Nomega-nitro-L-arginine methyl ester (L-NAME) blocked the increase in R
149                                   NG-nitro-L-arginine methyl ester (L-NAME) constricted and indometha
150 inhibitor L-N-iminoethyl lysine or N-nitro-L-arginine methyl ester (L-NAME) decreased the elevated pl
151 ed with the NO synthase inhibitor NG-nitro-l-arginine methyl ester (L-NAME) for 14 days plus Ang II d
152 lective NO synthase inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME) for 30 minutes, followed
153                     Infusion of N(G)-nitro-L-arginine methyl ester (L-NAME) for 5 min to inhibit NOS
154 eries was coated with 1 mmol/L of NG-nitro-L-arginine methyl ester (L-NAME) in 22% (wt/vol) Pluronic
155  oxide synthase (NOS) inhibitor N(6)-nitro-L-arginine methyl ester (L-NAME) in drinking water (NLN, I
156 the NO synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) increased sorbitol accumu
157                        In Site B, NG-nitro-L-arginine methyl ester (L-NAME) infusion during hyperther
158 sely, blockade of NOS using N(omega)-nitro-l-arginine methyl ester (l-NAME) inhibited l-arginine tran
159  of NO synthase inhibition with N(G)-nitro-L-arginine methyl ester (L-NAME) on the magnitude of the r
160 hours with 3 mM ATP or 2 mM N(omega)-nitro-L-arginine methyl ester (L-NAME) or 50 microM Reactive blu
161 e nitric oxide synthase inhibitor NW-nitro-L-arginine methyl ester (L-NAME) or its inactive isomer NW
162 pplication of the NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) or postsynaptic co-inject
163                    Molsidomine or NG-nitro-L-arginine methyl ester (L-NAME) or saline were applied da
164 e nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) or the ATP-sensitive mito
165 e report in this article that L-N(G)-nitro-L-arginine methyl ester (L-NAME) pretreatment blocked, whe
166 n of nitric oxide synthase with N(G)-nitro-L-arginine methyl ester (L-NAME) reduced maximal dilation
167       The NO synthase inhibitor N(G)-nitro-l-arginine methyl ester (L-NAME) significantly (P < 0.001)
168  solution infused in one probe and N-nitro-L-arginine methyl ester (L-NAME) through the second.
169 ted by either high glucose or Nomega-nitro-l-arginine methyl ester (L-NAME) treatment.
170                 L-arginine or Nomega-nitro-L-arginine methyl ester (L-NAME) was administered to stimu
171 ic oxide synthase inhibition by N(G)-nitro-L-arginine methyl ester (L-NAME) was much greater in LPS-t
172 ediated by nitric oxide (NO), Nomega-nitro-l-arginine methyl ester (l-NAME) was used.
173 oxide synthase (NOS) inhibitor N (G)-nitro-L-arginine methyl ester (L-NAME) worsened LV contractility
174 on of nitric oxide synthase (NOS) by nitro-L-arginine methyl ester (L-NAME) would alleviate the inhib
175 ol 1 (n = 10): (1) Control, (2) N(G)-nitro-l-arginine methyl ester (l-NAME), (3) a KCa channel inhibi
176 otocol: (1) ketorolac (Keto), (2) NG-nitro-l-arginine methyl ester (L-NAME), (3) Keto + l-NAME (Combo
177 s during steady state exercise (N(G)-nitro-L-arginine methyl ester (L-NAME), 25 mg over 5 min to inhi
178 sponse curves to acetylcholine, N(G)-nitro-L-arginine methyl ester (L-NAME), 8-bromo-cyclic 3',5'-gua
179  This activation was inhibited using l-nitro arginine methyl ester (L-NAME), a competitive inhibitor
180 rs was reduced in the presence of NG-nitro-L-arginine methyl ester (L-NAME), a general inhibitor of N
181 paw to block CGRP responses; N-omega-nitro-l-arginine methyl ester (L-NAME), a nonselective nitric-ox
182                                 N(w)-Nitro-l-arginine methyl ester (l-NAME), a nonspecific inhibitor
183 stration of either 100 mg/kg of N(G)-nitro-L-arginine methyl ester (L-NAME), a nonspecific NOS inhibi
184 n the absence or presence of N-Omega-nitro-L-arginine methyl ester (L-NAME), a specific NOS inhibitor
185 ncreased in the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric o
186     Chronic administration of Nomega-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric o
187                                 N(G)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synth
188                  Treatment with N(G)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NO synth
189 lished by application of either N(G)-nitro-l-arginine methyl ester (l-NAME), an inhibitor of NO synth
190                             N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NOS, sig
191                                    N-nitro-l-arginine methyl ester (L-NAME), an NO synthase inhibitor
192 nitric oxide synthase (NOS) inhibitor N(G)-L-arginine methyl ester (L-NAME), and compared its effects
193  by 7-nitro-indazole (7-NI) or N (G)-nitro-L-arginine methyl ester (L-NAME), completely prevented het
194 a nitric oxide synthase inhibitor, N-nitro-L-arginine methyl ester (L-NAME), on morphine hyperthermia
195 ing an inhibitor of nitric oxide, NG-nitro-L-arginine methyl ester (L-NAME), or a corresponding vehic
196  oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME), or by bilateral vagotomy
197 nine, nonspecific NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME), or iNOS selective inhibi
198 ected daily with either saline, N(G)-L-nitro-arginine methyl ester (L-NAME), or N-acetylcysteine for
199 d by a continuous infusion of Nomega-nitro-L-arginine methyl ester (L-NAME), or saline vehicle as con
200 ted, whereas the NOS inhibitor, N(G)-nitro-l-arginine methyl ester (L-NAME), potentiated LT release i
201 c oxide (NO) synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME), the guanylyl cyclase inh
202 nhibition in cancer cells using N(G)-nitro-l-arginine methyl ester (l-NAME), we demonstrate that pati
203                         Chronic N(G)-nitro-L-arginine methyl ester (L-NAME), which inhibits nitric ox
204    However, pretreatment of VEC with nitro-L-arginine methyl ester (L-NAME), while inhibiting the rel
205 hieved via systemic infusion of N(G)-nitro-l-arginine methyl ester (l-NAME), would reduce the gas exc
206                              In N(G)-nitro-L-arginine methyl ester (L-NAME)- and L-NAME+nifedipine-tr
207 times more superoxide by an N(omega)-nitro-L-arginine methyl ester (L-NAME)-inhibitable mechanism tha
208 nitric oxide synthase using N(omega)-nitro-L-arginine methyl ester (L-NAME)-recapitulates the numerou
209                      In wild-type, N-nitro-L-arginine methyl ester (L-NAME)-treated (with 1 mg/mL in
210 sed in isolated arterioles from N(G)-nitro-L-arginine methyl ester (L-NAME)-treated male and ovariect
211 onectomy but not by atropine or N(G)-nitro-l-arginine methyl ester (L-NAME).
212 se effects, mice were treated with N-nitro-L-arginine methyl ester (L-NAME).
213 e nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME).
214  the constitutive NOS inhibitor N(G)-nitro-l-arginine methyl ester (L-NAME).
215 roduced by systemic infusion of N(G)-nitro-L-arginine methyl ester (L-NAME).
216 long-term NOS inhibition by N(omega)-nitro-L-arginine methyl ester (L-NAME).
217 s of the NO synthase (NOS) inhibitor nitro-L-arginine methyl ester (L-NAME).
218 ion of nitric oxide synthesis with N-nitro-L-arginine methyl ester (L-NAME).
219 ficantly in the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME).
220 ith the NO synthase inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME).
221 ed NOS small molecule inhibitor N(G)-nitro-L-arginine methyl ester (l-NAME).
222 d by systemic pretreatment with L-N(G)-nitro arginine methyl ester (L-NAME).
223 vented by the eNOS inhibitor, Nomega-Nitro-L-arginine methyl ester (L-NAME).
224 nitric oxide synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME).
225 a nonselective NOS inhibitor [Nomega-nitro-L-arginine methyl ester (L-NAME)], or scavenging NO with a
226 ented by inhibition of NOS with N(G)-nitro-L-arginine methyl ester (L-NAME, 1 mM).
227 as tested by using the NOS inhibitor nitro-L-arginine methyl ester (L-NAME, 1 mmol/liter) in the pres
228 c oxide synthase (NOS) inhibitor, l-nitro(G)-arginine methyl ester (l-NAME, 1.5 mM), but was not affe
229 the nonspecific NOS inhibitor Nomega-nitro-L-arginine methyl ester (L-NAME, 10 mg/kg) in normal and s
230                 The addition of N(G)-nitro-L-arginine methyl ester (L-NAME, 10(-5) mM), an inhibitor
231 e presence of the NOS inhibitor N(G)-nitro-L-arginine methyl ester (l-NAME, 10(-5) mol l(-1)), the ar
232 he nitric oxide (NO) inhibitor N (G)-nitro-L-arginine methyl ester (L-NAME, 100 mg x kg(-1)) and the
233 hibiting NO synthase (NOS) with N(G)-nitro-L-arginine methyl ester (L-NAME, 250 microg/5 microl of ar
234                                   NG-nitro-L-arginine methyl ester (L-NAME, 300 microM), an inhibitor
235 ic oxide synthase inhibitor, N-omega-nitro-L-arginine methyl ester (L-NAME, 3x10(-4) mol/l), and sele
236 nistration of the NOS inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, 50 mg/kg/day) on energy i
237 f saline, GLP-2, and GLP-2 plus N(G)-Nitro-L-arginine methyl ester (L-NAME, 50 micromol x kg(-1) x ho
238 peroxide dismutase-mimetic), N-omega-nitro-L-arginine methyl ester (L-NAME, a nitric oxide synthase i
239                               The NG-nitro-L-arginine methyl ester (L-NAME, a NOS inhibitor), increas
240                    Microinjection of L-nitro-arginine methyl ester (L-NAME, an NO synthesis inhibitor
241 xamethonium (20 mg kg(-1)) and N (G)-nitro-L-arginine methyl ester (L-NAME; 10 mg kg(-1)), a nitric o
242  months with the NOS inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME; 10 mg/kg per day in drink
243                Treatment with Nomega-nitro-L-arginine methyl ester (L-NAME; 10(-4) mol/L), an NO synt
244         Inhibition of eNOS with N(G)-nitro-l-arginine methyl ester (l-NAME; 10(-6) M) completely inhi
245 cted instances, the NO synthase inhibitor, L-arginine methyl ester (L-NAME; 100 microM), or the NO do
246  oxide synthesis (NOS) inhibitor, NG-nitro-L-arginine methyl ester (L-NAME; 25 micromol/kg, i.v.) in
247 lial nitric oxide synthase with N(G)-nitro-L-arginine methyl ester (L-NAME; 300 microm) eliminated th
248 n of nitric oxide synthase with N(G)-nitro-L-arginine methyl ester (L-NAME; 300 microM).
249 s infusion of the NOS inhibitor N(G)-nitro-l-arginine methyl ester (l-NAME; 4 mg kg(1)), and for 120
250  intraperitoneally with saline, N(G)-nitro-L-arginine methyl ester (L-NAME; 8 mg/kg), or N(G)-nitro-D
251 ncomitant administration of LPS + NG-nitro-L-arginine methyl ester (L-NAME; an NO synthesis inhibitor
252  the NOS inhibitors ADMA or N(omega)-nitro-L-arginine methyl ester (L-NAME; each 250 micromol x kg(-1
253 hyl-L-arginine (L-NMMA; n = 6) or NG-nitro-L-arginine methyl ester (L-NAME; n = 8).
254 OS, L-NG-monomethyl arginine (L-NMMA), and L-arginine-methyl ester (L-NAME) had little or no effect o
255 ith incubation of NOS inhibitor N(G)-nitro-l-arginine-methyl ester (l-NAME) in LF-SED and HF-RUN grou
256      Inhibition of NOS with N(omega)-nitro-L-arginine-methyl ester (L-NAME) significantly increased c
257 the NO synthase (NOS) inhibitor N(G)-nitro-L-arginine-methyl ester (L-NAME), demonstrating the requir
258 ent of EC with NOS inhibitor, Nomega-nitro-L-arginine-methyl ester (L-NAME), significantly inhibited
259                      Addition of N G-nitro-l-arginine-methyl ester (L-NAME, 5 mM) to the probe perfus
260                              N omega-Nitro-L-arginine-methyl-ester (L-NAME) augmented the myogenic re
261 aboratory has demonstrated that N(G)-nitro-L-arginine-methyl-ester (L-NAME) mitigated cerebral ischem
262                               Nomega-nitro-L-arginine-methyl-ester (L-NAME) or placebo was administer
263 ring antagonism of NO synthase (N(G)-nitro-L-arginine methyl ester [L-NAME]) for 7, 14, or 21 days.
264 e and during NO inhibition (N(omega)-nitro-l-arginine methyl ester [L-NAME]).
265 own that inhibitors of NOS (N(omega)-nitro-L-arginine methyl ester [L-NAME], 7-nitroindazole [7-NI])
266 : NO synthase inhibition (10 mM N(G)-nitro-L-arginine methyl ester, L-NAME); low-dose NO infusion (1.
267  (with L-arginine) or blocking (with nitro-L-arginine methyl ester, (L-NAME)) NO synthesis could modu
268  specific NOS inhibitor L-NAME (N(G)-nitro-l-arginine methyl ester) led to increased APP and BACE1 (b
269 (NO) synthase inhibitor l-NAME (N(G)-nitro-l-arginine methyl ester) markedly inhibited the vasodilati
270 ther, the inhibition of eNOS (l-N(G)-nitro-L-arginine methyl ester), Mas (A-779), and SIRT1 (nicotina
271              The eNOS inhibitor N(G)-Nitro-l-arginine methyl ester mimicked anti-VEGF/VEGFR drugs, ra
272 ic oxide (NO) synthase with N(omega)-l-nitro-arginine-methyl ester (n = 5) significantly elevated mea
273 e performed on solutions containing N-acetyl arginine methyl ester, N-acetyl lysine methyl ester, gua
274 e (protein kinase C inhibitor), N(G)-nitro-L-arginine methyl ester (nitric oxide synthase inhibitor),
275                     L-NAME (N(omega)-nitro-L-arginine methyl ester; nitric oxide synthase inhibitor)
276  inhibitory effects of ADMA and N(G)-nitro-l-arginine methyl ester on inducible NOS (macrophages) and
277 ic-oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester or by the vanilloid VR1 receptor a
278  treatment of wild-type mice with NG-nitro-L-arginine methyl ester or loperamide prevented both the i
279 e nitric oxide synthase inhibitor N(omega)-L-arginine methyl ester or the xanthine oxidase inhibitor
280 ch was abolished by eNOS inhibitor N-nitro-L-arginine-methyl ester or H2O2 scavenger polyethylene gly
281  controls with NOS inhibited by N(G)-nitro-L-arginine methyl ester, or soluble guanylate cyclase (sGC
282  received 35 mg kg-1 day-1 of Nomega-nitro-L-arginine methyl ester orally for 10 days to inhibit NO s
283 de (NO) synthase inhibitor N(omega) -nitro-l-arginine methyl ester (P > 0.05), indicating that lower
284               Glibenclamide and N(G)-nitro-l-arginine methyl ester partially blocked the effect, indi
285 d that the small-molecule inhibitor, tosyl-l-arginine methyl ester, preferentially suppresses APC/C(C
286 h the NO synthase (NOS) inhibitor, N-nitro-l-arginine methyl ester prevented ischemia-induced AR acti
287                             N(omega)-nitro-l-arginine methyl ester reduced vasodilation to flow in ad
288            Inhibition of NOS by N(G)-nitro-l-arginine-methyl ester restored the ability of endotoxin
289 ionylation and eNOS-derived N(omega)-nitro-L-arginine methyl ester-sensitive superoxide formation in
290 lial nitric oxide synthase with N(G)-nitro-L-arginine methyl ester significantly attenuated the high
291  in vessels from rats treated with N-nitro-L-arginine methyl ester to increase blood pressure.
292                Furthermore, N(omega)-nitro-L-arginine methyl ester-treated or eNOS-deficient female m
293         When low-dose chronic Nomega-nitro-L-arginine methyl ester treatment was added for WF A/I-tre
294 fluoro-2-phenyl-1H-indol-3-yl)-1-oxobutyl]-L-arginine methyl ester trifluoroacetate) in M1 ipRGCs.
295   However, inhibition of NOS by N(G)-nitro-L-arginine methyl ester was accompanied by a sparing of CD
296 e HR, the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester was coinoculated with the avirulen
297  no further increases were seen when L-nitro-arginine-methyl ester was added.
298 -dansyl-N(omega)-(1,N(6)-etheno-ADP-ribosyl)-arginine methyl ester, was independent of redox potentia
299 or of nitric oxide synthesis L-NAME (L-nitro-arginine methyl ester), which had no effect of its own o
300 xide (NO) synthase inhibitor l-N (G)-nitro-l-arginine methyl ester, while iontophoresis of the NO don

 
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