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   1 medium supplemented with the arginine analog NG-nitro-L-arginine.                                    
     2 larly, NG-monomethyl-L-arginine 1 mmol/L and NG-nitro-L-arginine 10 micromol/L attenuated PSD by 57.5
     3  intact male mouse aortic rings treated with NG-nitro-L-arginine, 17 beta-estradiol caused dose-depen
     4 (C, Ringer solution), NOS-inhibited (10.0 mM NG-nitro-L-arginine), arginase-inhibited (5.0 mM (S)-(2-
     5  arginine site of cNOS, as assessed from [3H]NG-nitro-L-arginine binding, nor did they potently effec
  
     7 , but not SNAP, were blocked by 10(-4) mol/L NG-nitro-L-arginine, consistent with both BK and CCh sti
  
     9 venous infusion of the NO synthase inhibitor NG-nitro-L-arginine (L-NA, 13 mg/kg before the first occ
  
    11 The neutral nitric oxide synthase inhibitors NG-nitro-L-arginine (L-NNA) and N omega-monomethyl-L-arg
    12 effect of a nitric oxide synthase inhibitor, NG-nitro-L-arginine (L-NNA) on free radical generation a
  
    14 lium or addition of a NO synthase inhibitor, NG-nitro-L-arginine (LNNA), in control arteries decrease
    15 g(-1).min(-1) for 28 days) or treatment with NG-nitro-L-arginine methyl ester (1 mg/mL in drinking wa
    16  4 pigs after inhibition of NO synthase with NG-nitro-L-arginine methyl ester (1 to 2 mg/kg IV) had r
    17  (5 mumol/L), a cyclooxygenase inhibitor, or NG-nitro-L-arginine methyl ester (100 mumol/L), a nitric
    18 he nonselective NO* synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (100-800 nmol) as well 
  
  
    21 0 mm Hg from baseline, nine animals received NG-nitro-L-arginine methyl ester (L-NAME) at 15 mg/kg to
    22  of the rat mesentery with 50 micromol/liter NG-nitro-L-arginine methyl ester (L-NAME) caused a signi
  
    24 tric oxide (NO) generation with low doses of NG-nitro-L-arginine methyl ester (L-NAME) corrects the h
    25  were treated with the NO synthase inhibitor NG-nitro-l-arginine methyl ester (L-NAME) for 14 days pl
    26 onimine (SIN-1) or the NO synthase inhibitor NG-nitro-l-arginine methyl ester (L-NAME) in 12 control 
    27  of the arteries was coated with 1 mmol/L of NG-nitro-L-arginine methyl ester (L-NAME) in 22% (wt/vol
  
    29 on renal fibrosis, enalapril, enalapril plus NG-nitro-L-arginine methyl ester (L-NAME) or L-arginine 
    30 er the nitric oxide synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) or saline vehi
  
    32 bited by the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) or the ATP-sen
  
  
    35 anoid/NO protocol: (1) ketorolac (Keto), (2) NG-nitro-l-arginine methyl ester (L-NAME), (3) Keto + l-
    36 ied hemoglobin known to scavenge NO, and (2) NG-nitro-L-arginine methyl ester (L-NAME), a competitive
    37 RT activators was reduced in the presence of NG-nitro-L-arginine methyl ester (L-NAME), a general inh
    38 uncal vagotomy (TV), hexamethonium (C6), and NG-nitro-L-arginine methyl ester (L-NAME), but not by va
    39  administration of the general NOS inhibitor NG-nitro-L-arginine methyl ester (L-NAME), but not its d
    40 ich a nitric oxide synthase (NOS) inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), is neuroprote
    41 mps containing an inhibitor of nitric oxide, NG-nitro-L-arginine methyl ester (L-NAME), or a correspo
  
  
  
  
    46 erebroventricular (i.c.v.) administration of NG-nitro-l-arginine methyl ester (L-NAME; 150 microg/5 m
    47  the nitric oxide synthesis (NOS) inhibitor, NG-nitro-L-arginine methyl ester (L-NAME; 25 micromol/kg
    48 ally); a nonselective NO synthase inhibitor, Ng-nitro-L-arginine methyl ester (L-NAME; 30 mg/kg given
  
  
    51 onovaleric acid and by NO synthase inhibitor NG-nitro-L-arginine methyl ester and NG-monomethyl-L-arg
    52 s in nitrite, a response that was blocked by NG-nitro-L-arginine methyl ester and receptor-specific a
    53 er saline or treatment with a combination of NG-nitro-l-arginine methyl ester and sodium nitroprussid
    54 e treated with the nonspecific NOS inhibitor NG-nitro-L-arginine methyl ester and the NOS1-specific i
    55 tory effect of erythromycin was decreased by NG-nitro-L-arginine methyl ester and the vasoactive inte
  
    57 O synthase inhibitors N-nitro-L-arginine and NG-nitro-L-arginine methyl ester did not modify either b
    58 a greater percentage decrease in response to NG-Nitro-L-arginine methyl ester hydrochloride (L-NAME) 
    59 lated fibres with the NO synthase inhibitors NG-nitro-L-arginine methyl ester hydrochloride (L-NAME) 
  
  
    62 urthermore, treatment of wild-type mice with NG-nitro-L-arginine methyl ester or loperamide prevented
    63  abolished by the NO biosynthesis inhibitor (NG-nitro-L-arginine methyl ester) in the proximal and th
    64  before and after systemic administration of NG-nitro-L-arginine methyl ester, an arginine analogue k
  
  
    67 ated NO* with the competitive NOS inhibitor, NG-nitro-l-arginine methyl ester, in cells grown in l-ar
    68  administration of an NO synthase inhibitor, NG-nitro-L-arginine methyl ester, significantly inhibite
    69 THF reversed eNOS uncoupling, as assessed by NG-nitro-l-arginine methyl ester-inhibitable superoxide 
    70  5 x 10(-8) mol/L) caused a tetrodotoxin- or NG-nitro-L-arginine methyl ester-insensitive inhibition 
  
  
  
    74 e inducible nitric oxide synthase inhibitors Ng-nitro-L-arginine-methyl ester (1.5 mmol/L) and aminog
    75 g) of the nonselective NO synthase inhibitor NG-nitro-L-arginine-methyl ester (L-NAME) were administe
    76 odel, mice received daily i.p. injections of NG-nitro-L-arginine-methyl ester (L-NAME; 8 mg/kg) durin
  
  
    79 ence of the nitric oxide synthase inhibitor, NG-nitro-L-arginine or the endothelin B receptor antagon
  
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