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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
6                            Pretreatment with N omega-nitro-L-arginine methyl ester (100 micromol/L in
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
10                                              N(omega)-nitro-L-arginine methyl ester (30 microM) parti
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
13                            Moreover, l-NAME (N(omega)-nitro-l-arginine-methyl ester), a specific inhi
14                                              N(omega)-nitro-l-arginine methyl ester abolished the sys
15 ot differ significantly between groups after N omega-nitro-L-arginine methyl ester administration.
16                  The inhibition of eNOS with N-omega-nitro-L-arginine methyl ester also potently redu
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
21                                              N(omega)-Nitro-L-arginine methyl ester and 1H-[1,2,4]-ox
22 ence of the nitric oxide synthase inhibitors N-omega-nitro-L-arginine methyl ester and S-methyl-thioc
23 -DAMP, charybdotoxin or BAPTA-AM, but not by N(omega)-nitro-L-arginine methyl ester, glipizide, indom
24 arterioles pretreated with ceramide, whereas N(omega)-nitro-l-arginine methyl ester had no effect.
25                                              N(omega)-Nitro-L-arginine methyl ester, HOE-140, and dic
26 epeated hypertensive challenges using either N(omega)-nitro-L-arginine methyl ester hydrochloride (L-
27  In the presence of DTT and the NO inhibitor N(omega)-nitro-L-arginine methyl ester hydrochloride, th
28 ing nitric oxide (NO) synthesis with L-NAME (N(omega)-nitro-L-arginine methyl ester hydrochloride; 5
29 y the competitive inhibitor of NO synthesis, N omega-nitro-L-arginine methyl ester, indicating that A
30       Mechanistically, blockade of eNOS with N(omega)-nitro-L-arginine methyl ester ( L-NAME) abolish
31 with a nitric oxide (NO) synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME) or 7-nitr
32  demand after the systemic administration of N omega-nitro-L-arginine methyl ester (L-NAME) or N omeg
33    NOS inhibitors 7-nitroindazole (7-NI) and N omega-nitro-L-arginine methyl ester (L-NAME) produced
34                   Furthermore, (100 mumol/L) N omega-nitro-L-arginine methyl ester (L-NAME), a nitric
35 ine and the nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME), an incre
36 d NG-monomethyl-L-arginine (L-NMMA), but not N omega-nitro-L-arginine methyl ester (L-NAME), trans-st
37  1-arginine, indomethacin, meclofenamate, or N omega-nitro-L-arginine methyl ester (L-NAME).
38  nitric oxide (NO) was inhibited by 10(-4) M N omega-nitro-L-arginine methyl ester (L-NAME).
39 0(-5) mol/L; a cyclooxygenase inhibitor) and N omega-nitro-L-arginine methyl ester (L-NAME, 10(-4) mo
40 N omega-nitro-L-argininel-NA; 100 microM) or N omega-nitro-L-arginine methyl ester (L-NAME; 100 micro
41  and systemic inhibition of endogenous NO by N omega-nitro-L-arginine methyl ester (L-NAME; 100 mumol
42                                 At 190 mins, N omega-nitro-L-arginine methyl ester (L-NAME; 10mg/kg)
43                                              N omega-Nitro-L-arginine-methyl-ester (L-NAME) augmented
44                            Pretreatment with N(omega)-nitro-l-arginine methyl ester (l-NAME) (10(-3)
45 o to 25 mM, but was unaffected by 100 microM N(omega)-nitro-L-arginine methyl ester (L-NAME) (68 +/-
46  was completely abolished in the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME) (a nitri
47 ivity and, conversely, blockade of NOS using N(omega)-nitro-l-arginine methyl ester (l-NAME) inhibite
48  treated for 3.5 hours with 3 mM ATP or 2 mM N(omega)-nitro-L-arginine methyl ester (L-NAME) or 50 mi
49  rats was determined after administration of N(omega)-nitro-L-arginine methyl ester (L-NAME) or salin
50                                              N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhi
51 e substantially increased in the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME), an inhi
52 arts generated 3 times more superoxide by an N(omega)-nitro-L-arginine methyl ester (L-NAME)-inhibita
53 ular response to long-term NOS inhibition by N(omega)-nitro-L-arginine methyl ester (L-NAME).
54 e increased significantly in the presence of N(omega)-nitro-L-arginine methyl ester (L-NAME).
55                            Administration of N(omega)-nitro-L-arginine methyl ester (L-NAME; 20 mg/kg
56 ith either PBS or the NOS inhibitors ADMA or N(omega)-nitro-L-arginine methyl ester (L-NAME; each 250
57                       Inhibition of NOS with N(omega)-nitro-L-arginine-methyl ester (L-NAME) signific
58          Prior treatment of the ganglia with N-omega-nitro-L-arginine methyl ester (L-NAME), a nitric
59 to the left hindpaw to block CGRP responses; N-omega-nitro-l-arginine methyl ester (L-NAME), a nonsel
60 ith native LDL in the absence or presence of N-Omega-nitro-L-arginine methyl ester (L-NAME), a specif
61 travenously) with the NO synthase inhibitor, N-omega-nitro-L-arginine methyl ester (L-NAME), or the c
62             Nitric oxide synthase inhibitor, N-omega-nitro-L-arginine methyl ester (L-NAME, 3x10(-4)
63 xyl (TEMPOL,a superoxide dismutase-mimetic), N-omega-nitro-L-arginine methyl ester (L-NAME, a nitric
64 re measured before and during NO inhibition (N(omega)-nitro-l-arginine methyl ester [L-NAME]).
65 e have earlier shown that inhibitors of NOS (N(omega)-nitro-L-arginine methyl ester [L-NAME], 7-nitro
66 (Pe), sodium nitroprusside (Snp) with Pe, or N omega-nitro-L-arginine methyl ester (Lnam).
67 diator or NO released despite treatment with N(omega)-nitro-L-arginine methyl ester, N(omega)-nitro-L
68 utaneous administration of 10 micrograms/min N omega-nitro-L-arginine methyl ester (NAME) for 48 hour
69 ffects were totally reversed by provision of N(omega)-nitro-L-arginine methyl ester (NAME) in arginin
70                                      L-NAME (N(omega)-nitro-L-arginine methyl ester; nitric oxide syn
71  and O2 consumption in vitro were blocked by N omega-nitro-L-arginine methyl ester or N omega-nitro-L
72 t not by the nitric-oxide synthase inhibitor N(omega)-nitro-L-arginine methyl ester or by the vanillo
73 ith the nitric oxide (NO) synthase inhibitor N(omega) -nitro-l-arginine methyl ester (P > 0.05), indi
74                                              N(omega)-nitro-l-arginine methyl ester reduced vasodilat
75 tion of the nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester, reverses the vaso
76 nted eNOS glutathionylation and eNOS-derived N(omega)-nitro-L-arginine methyl ester-sensitive superox
77                  After the administration of N omega-nitro-L-arginine methyl ester, systemic vascular
78                            Pretreatment with N omega-nitro-L-arginine methyl ester to block NO synthe
79                                 Furthermore, N(omega)-nitro-L-arginine methyl ester-treated or eNOS-d

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