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1 y-L-arginine, N omega-methyl-L-arginine, and N omega-nitro-L-arginine.
2 ga-nitro-L-arginine methyl ester (L-NAME) or N omega-nitro-L-arginine.
3 r stress and was blocked by the NO inhibitor N(omega)-nitro-L-arginine.
4 by the nitric oxide (NO) synthase inhibitors N(omega)-nitro-L-arginine (10 mg/kg) or N(omega)-nitro-L
5 that were unaffected by endothelium removal, N(omega)-nitro-L-arginine (10(- 4) mol/L, an NO synthase
7 n response to acetylcholine was inhibited by N(omega)-nitro-L-arginine (100 micromol/L) in all groups
10 iments, the nitric oxide synthase inhibitor, N omega-nitro-L-arginine (3 x 10(-4) M), was added to th
12 was enhanced by arginine analogs, including N(omega)-nitro-l-arginine (a NO synthase inhibitor), sug
15 ino-sydonimine) nor a NO synthase inhibitor (N omega-nitro-L-arginine) altered FMLP- or IL-8-elicited
18 hibition of nitric oxide synthase (NOS) with N(omega)-nitro-L-arginine during the 30-minute occlusion
19 urred after the administration of L-NAME and N omega-nitro-L-arginine in chronically instrumented ani
20 by N omega-nitro-L-arginine methyl ester or N omega-nitro-L-arginine, inhibitors of endogenous NO fo
21 nhibition of any of the NOS isoforms, unlike N omega-nitro-L-arginine itself, which does, although it
22 The nitric oxide (NO) synthase inhibitor N omega -nitro-L-arginine (L-NA, 100 microM; n = 16) abo
23 arginine and group 4 received L-arginine and N omega-nitro-L-arginine (L-NA), an inhibitor of NO synt
27 ild-type mice treated with the NOS inhibitor N(omega)-nitro L-arginine (L-NA) and eNOS-deficient mice
28 ts were given the nonselective NOS inhibitor N(omega)-nitro-L-arginine (L-NA, 13 mg/kg i.v. [group II
29 temic nitric oxide synthase inhibition using N(omega)-nitro-L-arginine (L-NA, 30 mg/kg for 3 days), r
30 lockade of inhibitory neurotransmission with N(omega)-nitro-L-arginine (L-NA, a NO synthesis inhibito
32 deoxycorticosterone acetate (DOCA)-salt and N(omega)-nitro-L-arginine (L-NNA) hypertensive but not n
33 nitric oxide synthase (NOS) inhibition using N(omega)-nitro-L-arginine (L-NNA) was also assessed, bec
35 d before and after the NO synthase inhibitor N(omega)-nitro-L-arginine (L-NNA), L-NNA plus L-citrulli
38 rotoporphyrin IX [SnPP IX] for CO synthesis, N(omega)-nitro-L-arginine [L-NNA] for NO synthesis, and
39 cible nitric oxide synthase (iNOS) inhibitor N(omega)-nitro-L-arginine(L-NNA) induced E-selectin expr
40 the local (direct) response was inhibited by N(omega)-nitro-L-arginine (LNA), and both local and cond
41 A(2) adenosine receptors, 10(-4) or 10(-3) M N(omega)-nitro-L-arginine (LNNA) to block nitric oxide p
43 ion with the nitric oxide synthase inhibitor N omega-nitro-L-arginine methyl ester (11.2 +/- 3.7% inc
44 olus of the nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester (25 mg/kg), after
45 with a nitric oxide (NO) synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME) or 7-nitr
46 demand after the systemic administration of N omega-nitro-L-arginine methyl ester (L-NAME) or N omeg
47 NOS inhibitors 7-nitroindazole (7-NI) and N omega-nitro-L-arginine methyl ester (L-NAME) produced
49 ine and the nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME), an incre
50 d NG-monomethyl-L-arginine (L-NMMA), but not N omega-nitro-L-arginine methyl ester (L-NAME), trans-st
53 0(-5) mol/L; a cyclooxygenase inhibitor) and N omega-nitro-L-arginine methyl ester (L-NAME, 10(-4) mo
54 N omega-nitro-L-argininel-NA; 100 microM) or N omega-nitro-L-arginine methyl ester (L-NAME; 100 micro
55 and systemic inhibition of endogenous NO by N omega-nitro-L-arginine methyl ester (L-NAME; 100 mumol
58 utaneous administration of 10 micrograms/min N omega-nitro-L-arginine methyl ester (NAME) for 48 hour
59 ot differ significantly between groups after N omega-nitro-L-arginine methyl ester administration.
60 and O2 consumption in vitro were blocked by N omega-nitro-L-arginine methyl ester or N omega-nitro-L
62 y the competitive inhibitor of NO synthesis, N omega-nitro-L-arginine methyl ester, indicating that A
63 tion of the nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester, reverses the vaso
65 ith the nitric oxide (NO) synthase inhibitor N(omega) -nitro-l-arginine methyl ester (P > 0.05), indi
68 10(-5) mol/L), a transcription inhibitor; or N(omega)-nitro-L-arginine methyl ester (10(-4) mol/L), a
69 tors N(omega)-nitro-L-arginine (10 mg/kg) or N(omega)-nitro-L-arginine methyl ester (20 mg/kg) and th
72 o to 25 mM, but was unaffected by 100 microM N(omega)-nitro-L-arginine methyl ester (L-NAME) (68 +/-
73 was completely abolished in the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME) (a nitri
74 ivity and, conversely, blockade of NOS using N(omega)-nitro-l-arginine methyl ester (l-NAME) inhibite
75 treated for 3.5 hours with 3 mM ATP or 2 mM N(omega)-nitro-L-arginine methyl ester (L-NAME) or 50 mi
76 rats was determined after administration of N(omega)-nitro-L-arginine methyl ester (L-NAME) or salin
78 e substantially increased in the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhi
79 arts generated 3 times more superoxide by an N(omega)-nitro-L-arginine methyl ester (L-NAME)-inhibita
83 ith either PBS or the NOS inhibitors ADMA or N(omega)-nitro-L-arginine methyl ester (L-NAME; each 250
84 ffects were totally reversed by provision of N(omega)-nitro-L-arginine methyl ester (NAME) in arginin
86 e have earlier shown that inhibitors of NOS (N(omega)-nitro-L-arginine methyl ester [L-NAME], 7-nitro
89 arterioles pretreated with ceramide, whereas N(omega)-nitro-l-arginine methyl ester had no effect.
90 epeated hypertensive challenges using either N(omega)-nitro-L-arginine methyl ester hydrochloride (L-
91 In the presence of DTT and the NO inhibitor N(omega)-nitro-L-arginine methyl ester hydrochloride, th
92 ing nitric oxide (NO) synthesis with L-NAME (N(omega)-nitro-L-arginine methyl ester hydrochloride; 5
93 t not by the nitric-oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester or by the vanillo
95 signal regulated kinase (ERK) inhibitor, and N(omega)-nitro-L-arginine methyl ester, an antagonist of
96 ose-induced NOX4 expression was abrogated by N(omega)-nitro-l-arginine methyl ester, an inhibitor of
97 However, intracerebroventricular infusion of N(omega)-nitro-L-arginine methyl ester, an inhibitor of
98 -DAMP, charybdotoxin or BAPTA-AM, but not by N(omega)-nitro-L-arginine methyl ester, glipizide, indom
100 diator or NO released despite treatment with N(omega)-nitro-L-arginine methyl ester, N(omega)-nitro-L
101 nted eNOS glutathionylation and eNOS-derived N(omega)-nitro-L-arginine methyl ester-sensitive superox
106 retreated with a nonselective NOS inhibitor (N(omega)-nitro-L-arginine methyl ester; 30 mg/kg), a sol
109 to the left hindpaw to block CGRP responses; N-omega-nitro-l-arginine methyl ester (L-NAME), a nonsel
110 ith native LDL in the absence or presence of N-Omega-nitro-L-arginine methyl ester (L-NAME), a specif
111 travenously) with the NO synthase inhibitor, N-omega-nitro-L-arginine methyl ester (L-NAME), or the c
113 xyl (TEMPOL,a superoxide dismutase-mimetic), N-omega-nitro-L-arginine methyl ester (L-NAME, a nitric
115 (NOS) inhibitors 7-nitroindazole (7-NI) and N-omega-nitro-L-arginine methyl ester also reduced NMDA
116 ence of the nitric oxide synthase inhibitors N-omega-nitro-L-arginine methyl ester and S-methyl-thioc
117 ment with a nitric oxide synthase inhibitor (N-omega-nitro-L-arginine methyl ester, 50 mg/kg/day) or
122 ts of the nonselective NO synthase inhibitor N(omega)-nitro L-arginine methylester (L-NAME) in health
123 reated intraperitoneally with either L-NAME (N-omega-nitro-L-arginine methylester), a competitive inh
127 bsence of nitric oxide synthetase inhibitor, N omega-nitro-L-arginine (NLA), was investigated in Mong
128 g to the equivalent complexes of nNOS, while N(omega)-nitro-L-arginine (NNA) binding produces a state
129 orn piglet brains and that pretreatment with N(omega)-nitro-L-arginine (NNLA), an inhibitor of nitric
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