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1 s well as when NO synthesis was inhibited by N(omega)-nitro-l-arginine methyl ester.
2 ent with the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester.
3 e was abolished by chronic administration of N(omega)-nitro-L-arginine methyl ester.
4 til inhibition of nitric oxide synthase with N(omega) -nitro-l-arginine methyl ester.
5 10(-5) mol/L), a transcription inhibitor; or N(omega)-nitro-L-arginine methyl ester (10(-4) mol/L), a
7 ion with the nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester (11.2 +/- 3.7% inc
8 tors N(omega)-nitro-L-arginine (10 mg/kg) or N(omega)-nitro-L-arginine methyl ester (20 mg/kg) and th
9 olus of the nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester (25 mg/kg), after
11 retreated with a nonselective NOS inhibitor (N(omega)-nitro-L-arginine methyl ester; 30 mg/kg), a sol
12 ment with a nitric oxide synthase inhibitor (N-omega-nitro-L-arginine methyl ester, 50 mg/kg/day) or
15 ot differ significantly between groups after N omega-nitro-L-arginine methyl ester administration.
17 (NOS) inhibitors 7-nitroindazole (7-NI) and N-omega-nitro-L-arginine methyl ester also reduced NMDA
18 signal regulated kinase (ERK) inhibitor, and N(omega)-nitro-L-arginine methyl ester, an antagonist of
19 ose-induced NOX4 expression was abrogated by N(omega)-nitro-l-arginine methyl ester, an inhibitor of
20 However, intracerebroventricular infusion of N(omega)-nitro-L-arginine methyl ester, an inhibitor of
22 ence of the nitric oxide synthase inhibitors N-omega-nitro-L-arginine methyl ester and S-methyl-thioc
23 red blood pressure with radiotelemetry after N-omega-nitro-L-arginine-methyl ester and a high salt di
24 -DAMP, charybdotoxin or BAPTA-AM, but not by N(omega)-nitro-L-arginine methyl ester, glipizide, indom
25 arterioles pretreated with ceramide, whereas N(omega)-nitro-l-arginine methyl ester had no effect.
27 epeated hypertensive challenges using either N(omega)-nitro-L-arginine methyl ester hydrochloride (L-
28 mouse model (induced by a high-fat diet plus N(omega)-nitro-L-arginine methyl ester hydrochloride [L-
29 c oxide production by oral administration of N(omega)-Nitro-L-arginine methyl ester hydrochloride, an
30 In the presence of DTT and the NO inhibitor N(omega)-nitro-L-arginine methyl ester hydrochloride, th
31 ing nitric oxide (NO) synthesis with L-NAME (N(omega)-nitro-L-arginine methyl ester hydrochloride; 5
32 y the competitive inhibitor of NO synthesis, N omega-nitro-L-arginine methyl ester, indicating that A
34 with a nitric oxide (NO) synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME) or 7-nitr
35 demand after the systemic administration of N omega-nitro-L-arginine methyl ester (L-NAME) or N omeg
36 NOS inhibitors 7-nitroindazole (7-NI) and N omega-nitro-L-arginine methyl ester (L-NAME) produced
38 ine and the nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME), an incre
39 d NG-monomethyl-L-arginine (L-NMMA), but not N omega-nitro-L-arginine methyl ester (L-NAME), trans-st
42 0(-5) mol/L; a cyclooxygenase inhibitor) and N omega-nitro-L-arginine methyl ester (L-NAME, 10(-4) mo
43 N omega-nitro-L-argininel-NA; 100 microM) or N omega-nitro-L-arginine methyl ester (L-NAME; 100 micro
44 and systemic inhibition of endogenous NO by N omega-nitro-L-arginine methyl ester (L-NAME; 100 mumol
48 o to 25 mM, but was unaffected by 100 microM N(omega)-nitro-L-arginine methyl ester (L-NAME) (68 +/-
49 was completely abolished in the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME) (a nitri
50 ivity and, conversely, blockade of NOS using N(omega)-nitro-l-arginine methyl ester (l-NAME) inhibite
51 treated for 3.5 hours with 3 mM ATP or 2 mM N(omega)-nitro-L-arginine methyl ester (L-NAME) or 50 mi
52 rats was determined after administration of N(omega)-nitro-L-arginine methyl ester (L-NAME) or salin
54 e substantially increased in the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhi
55 arts generated 3 times more superoxide by an N(omega)-nitro-L-arginine methyl ester (L-NAME)-inhibita
56 of constitutive nitric oxide synthase using N(omega)-nitro-L-arginine methyl ester (L-NAME)-recapitu
60 ith either PBS or the NOS inhibitors ADMA or N(omega)-nitro-L-arginine methyl ester (L-NAME; each 250
63 to the left hindpaw to block CGRP responses; N-omega-nitro-l-arginine methyl ester (L-NAME), a nonsel
64 ith native LDL in the absence or presence of N-Omega-nitro-L-arginine methyl ester (L-NAME), a specif
65 travenously) with the NO synthase inhibitor, N-omega-nitro-L-arginine methyl ester (L-NAME), or the c
67 xyl (TEMPOL,a superoxide dismutase-mimetic), N-omega-nitro-L-arginine methyl ester (L-NAME, a nitric
69 e have earlier shown that inhibitors of NOS (N(omega)-nitro-L-arginine methyl ester [L-NAME], 7-nitro
71 diator or NO released despite treatment with N(omega)-nitro-L-arginine methyl ester, N(omega)-nitro-L
72 utaneous administration of 10 micrograms/min N omega-nitro-L-arginine methyl ester (NAME) for 48 hour
73 ffects were totally reversed by provision of N(omega)-nitro-L-arginine methyl ester (NAME) in arginin
75 and O2 consumption in vitro were blocked by N omega-nitro-L-arginine methyl ester or N omega-nitro-L
76 t not by the nitric-oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester or by the vanillo
77 ith the nitric oxide (NO) synthase inhibitor N(omega) -nitro-l-arginine methyl ester (P > 0.05), indi
79 tion of the nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester, reverses the vaso
80 nted eNOS glutathionylation and eNOS-derived N(omega)-nitro-L-arginine methyl ester-sensitive superox
84 FD+L-NAME (ad libitum high-fat diet and 0.5% N[omega]-nitro-L-arginine methyl ester), we observe that