ライフサイエンスコーパス: NG-monomethyl-L-arginine

1 , glyceryl trinitrate, norepinephrine, and l-NG-monomethyl-l-arginine.

2 by the nitric oxide synthase (NOS) inhibitor NG-monomethyl-l-arginine.

3 hibitor NG-nitro-L-arginine methyl ester and NG-monomethyl-L-arginine.

4 oxide (NO) was seen that could be blocked by NG-monomethyl-L-arginine.

5 ition of the nitric oxide synthase inhibitor NG-monomethyl-L-arginine.

6 eased with the addition of the NOS inhibitor NG-monomethyl-L-arginine.

7 inhibitory effect was comparable to that of NG-monomethyl-L-arginine.

8 inhibitor of inducible NO. synthase (iNOS), NG-monomethyl-L-arginine.

9 ction in these cells, which was inhibited by NG-monomethyl-L-arginine.

10 ed by a competitive inhibitor of NO synthase NG-monomethyl-L-arginine.

11 nt could not be blocked by the NOS inhibitor NG-monomethyl-L-arginine.

12 Similarly, NG-monomethyl-L-arginine 1 mmol/L and NG-nitro-L-arginin

13 In the presence of the NO synthase inhibitor NG-monomethyl-L-arginine (1 mmol/L), both SFLLRN- and SL

14 sion with a nitric oxide synthase inhibitor, NG-monomethyl-L-arginine (10 or 100 micromol l-1), nor t

15 In controls, NG-monomethyl-L-arginine (100 microM) reduced basal +dP/

16 14.9+/-1.5 mL.min-1.dL-1; P=0.006) and after NG-monomethyl-L-arginine (6.1+/-1.2 versus 10.1+/-0.8 mL

17 kis [4-benzoic acid]) porphyrin and l -NMMA (NG-monomethyl-l -arginine), a superoxide dismutase mimet

18 r the synthesis of nitric oxide, and L-NMMA (NG-monomethyl-L-arginine), a nitric oxide synthase block

19 on of the endothelium, and administration of NG-monomethyl-L-arginine abrogated the stimulatory effec

20 fusion (P=0.01) but not further increased by NG-monomethyl-L-arginine acetate (P=0.2).

21 conversion of l-arginine to l-citrulline by NG-monomethyl-l-arginine acetate, a specific inhibitor o

22 Blockade of nitric-oxide synthase (NOS) with NG-monomethyl-L-arginine acetate, and cGMP with RpcGMP,

23 NG-monomethyl-L-arginine, an inhibitor of nitric oxide (

24 F-alpha was lost either after treatment with NG-monomethyl-l-arginine, an inhibitor of NO production,

25 were inhibited by the NO synthase inhibitor NG-monomethyl-L-arginine and were subsequently reversed

26 c oxide (NO), since the in vitro addition of NG-monomethyl-L-arginine blocked suppression.

27 mic treatment of mice with the NOS inhibitor NG-monomethyl-l-arginine delayed weight loss and death a

28 nding that the frequently used NOS inhibitor NG-monomethyl L-arginine enhanced O-2 production in the

29 de or by the nitric oxide synthase inhibitor NG-monomethyl-l-arginine, fluorescence recovery was sign

30 lso improved by NOS inhibition (P<0.01), and NG-monomethyl-L-arginine infusion slightly prolonged gra

31 F-alpha) neutralizing antibody or 200 microM NG-monomethyl-L-arginine (L-NGMMA), a competitive inhibi

32 NG-monomethyl-L-arginine (L-NMA) potentiated the increas

33 l/l), and/or the NO synthase (NOS) inhibitor NG-monomethyl-L-arginine (L-NMMA) (0.1 mmol/l).

34 ce and absence of the NO synthase antagonist NG-monomethyl-l-arginine (l-NMMA) (0.3 mg/kg/min intrave

35 ion after 2 h (but not 1 h) was abolished by NG-monomethyl-l-arginine (l-NMMA) and 2-amino-5,6-dihydr

36 hibition of nitric oxide synthase (NOS) with NG-monomethyl-L-arginine (L-NMMA) causes acute insulin r

37 ed relaxations similarly in both groups, but NG-monomethyl-L-arginine (L-NMMA) did not inhibit relaxa

38 inine methyl ester hydrochloride (L-NAME) or NG-monomethyl-L-arginine (L-NMMA) reduced the increase i

39 When the nitric oxide synthase blocker NG-monomethyl-L-arginine (L-NMMA) was administered in th

40 After the 4-h sample period, NG-monomethyl-L-arginine (L-NMMA) was infused into the b

41 NG-Monomethyl-L-arginine (L-NMMA) was used as a specific

42 Inhibition of cGMP production with NG-monomethyl-L-arginine (L-NMMA), a competitive inhibit

43 The hemodynamic effects of NG-monomethyl-L-arginine (L-NMMA), a nitric oxide syntha

44 L-arginine and NG-monomethyl-L-arginine (L-NMMA), but not N omega-nitro

45 rt FFA elevation blunted the LBF response to NG-monomethyl-L-arginine (L-NMMA), which is an inhibitor

46 nitroprusside, and the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA).

47 ebs solution alone or with the NO-inhibitor, NG-monomethyl-L-arginine (L-NMMA).

48 P, and sodium nitroprusside before and after NG-monomethyl-L-arginine (L-NMMA).

49 ed using the nitric oxide synthase inhibitor NG-monomethyl-L-arginine (L-NMMA); and nitroprusside was

50 Conversely, treatment with NG-monomethyl-L-arginine (L-NMMA, 1 mM), an inhibitor of

51 sed with the nitric oxide synthase inhibitor NG-monomethyl-l-arginine (l-NMMA, 10 mm), the non-select

52 ide and prostaglandins was assessed by using NG-monomethyl-L-arginine (L-NMMA, 10 mumol/L) and indome

53 acin (5 mg/kg to inhibit cyclooxygenase), or NG-monomethyl-L-arginine (L-NMMA, 100 mg/kg, to inhibit

54 kg, n = 8) or with the NO synthase inhibitor NG-monomethyl-L-arginine (L-NMMA, 30 mg/kg, n = 7) befor

55 his sequence during coinfusion of saline and NG-monomethyl-L-arginine (L-NMMA, 4 mumol.min-1), an inh

56 -homoarginine (which is not metabolized) and NG-monomethyl-L-arginine (L-NMMA, a nitric oxide synthas

57 cts were completely reversed with a 1 mmol/L NG-monomethyl-L-arginine (L-NMMA, a NO synthase inhibito

58 (agonists that stimulate NO production) and NG-monomethyl-L-arginine (L-NMMA, an inhibitor of NO pro

59 ynthase (NOS) was competitively inhibited by NG-monomethyl-L-arginine (L-NMMA; 0.5 mg kg-1, intracoro

60 pial arterioles, we examined the effects of NG-monomethyl-L-arginine (L-NMMA; 10 microM).

61 t was affected by the NO synthase inhibitors NG-monomethyl-L-arginine (L-NMMA; 100 micromol/l) or 7-n

62 g the concurrent blockade of NO synthesis by NG-monomethyl-L-arginine (L-NMMA; 4 micromol/min).

63 An inhibitor of nitric oxide synthase (NOS), NG-monomethyl-L-arginine (L-NMMA; 50 micromoles/kg body

64 lar responses to intra-arterial infusions of NG-monomethyl-l-arginine (l-NMMA; an inhibitor of NO syn

65 ses were not restored by NOS inhibition with NG-monomethyl-L-arginine (L-NMMA; n = 6) or NG-nitro-L-a

66 oxide synthase by in vitro administration of NG-monomethyl-L-arginine (L-NNMMA) did not alter the H2O

67 entolamine and yohimbine), and nitric oxide (NG-monomethyl-L-arginine, L-NMMA) regulation of blood fl

68 fusion (control) and NO synthase inhibition (NG-monomethyl-L-arginine; L-NMMA) under normoxic and nor

69 ) before and after NO synthase blockade with NG-monomethyl-L-arginine (LNNA, 1.5 mg/kg IC).

70 Studies using NG-monomethyl-L-arginine monoacetate, an inhibitor of ni

71 te (DETA-NO), and the NO synthase inhibitor, NG-monomethyl-L-arginine.monoacetate (L-NMMA), showed th

72 Specifically, administration of NG-monomethyl-l -arginine (NGMMA) via osmotic pumps incr

73 cible nitric oxide synthase (iNOS) inhibitor NG-monomethyl-L-arginine (NGMMLA) or the H2O2 scavenger

74 cked by the nitric oxide synthase inhibitors NG-monomethyl-L-arginine, nitroarginine, and aminoguanid

75 e adjuvant effect of RBC was not modified by NG-monomethyl-L-arginine (NMA, an NO synthase inhibitor)

76 hown to be mediated by nitric oxide (NO), as NG-monomethyl-L-arginine (NMMA) gave complete reversal o

77 he inhibitor of nitric oxide synthase (NOS), NG-monomethyl-L-arginine (NMMA).

78 ynthesis was inhibited by the NOS inhibitors NG-monomethyl-L-arginine or N-3-aminoethylbenzylacetamid

79 In myocytes, the NO synthase inhibitor NG-monomethyl-L-arginine potentiated NE-stimulated [3H]l

80 Inhibition of NO synthesis by NG-monomethyl-L-arginine produced dose-dependent attenua

81 e killing of M. smegmatis was not blocked by NG-monomethyl-L-arginine, suggesting that it was not due

82 e cells and that this effect is inhibited by NG-monomethyl-L-arginine, suggesting that vitamin D-indu

83 ainst opsonized rickettsiae was inhibited by NG-monomethyl-L-arginine, superoxide dismutase, catalase

84 es by opsonized rickettsiae was inhibited by NG-monomethyl-L-arginine, superoxide dismutase, mannitol

85 ortterm treatment of TGF-beta 1-/- mice with NG-monomethyl-L-arginine suppressed this elevated produc

86 ity and forearm vasoconstrictor responses to NG-monomethyl-L-arginine, the substrate inhibitor of nit

87 lity of cycloheximide or the arginine analog NG-monomethyl-L-arginine to abolish NO production; the e

88 n was accomplished by continuous infusion of NG-monomethyl-L-arginine via a subcutaneous osmotic pump