ライフサイエンスコーパス: L-NNA

1 L-NNA abolished C-peptide effects on nerve conduction.

2 L-NNA and nNOS deletion (approximately 80%) and VIP(10-2

3 L-NNA area under the curve (AUC) increased linearly with

4 L-NNA failed to inhibit this response, however, and did

5 L-NNA prevented luminal filopodia and vacuolisation in r

6 L-NNA reduced the magnitude of the AFC response (p<0.05)

7 L-NNA treatment or endothelial NOS (eNOS) gene deletion,

8 L-NNA, a nitric oxide (NO) synthase inhibitor, and Rp 8-

9 to 4.0 +/- 1.2 nmol/l, a 25% rise (p < 0.01, L-NNA vs. control).

10 ntervals (20 s) was augmented (p<0.05) after L-NNA.

11 +/-1 vs. 11+/-1 and 18+/-1% before and after L-NNA 10(-3) M).

12 duction in tumour blood volume at 24 h after L-NNA (r=0.83; p=0.010).

13 tant (K) were measured at 1 h and 24 h after L-NNA administration.

14 ing, tumour blood volume decreased 1 h after L-NNA treatment (mean 42.9% [range 12.0-62.1]; paired t

15 n oscillations (0.17 Hz) were observed after L-NNA administration.

16 ry for coronary vasodilation before or after L-NNA.

17 Simultaneous administration of INDO and L-NNA eliminated flow-induced responses in arterioles of

18 e of smaller amplitude in W/W(V) muscles and L-NNA did not attenuate relaxation responses in W/W(V) f

19 line cholinergic tone of the trachealis, and L-NNA potentiated histamine-induced contractions of the

20 The effects of TTX and L-NNA were not additive, however, suggesting that the tw

21 lial nitric oxide synthase (eNOS) antagonist L-NNA and its agonist scutellarin, hemoglobin, DETA/NO (

22 hase (NOS) inhibitor, N(G)-nitro-L-arginine (L-NNA) (40 mg/kg).

23 Administration of NG-nitro-L-arginine (L-NNA) abolished the increase in capillary to fibre rati

24 ide synthase inhibitors NG-nitro-L-arginine (L-NNA) and N omega-monomethyl-L-arginine (L-NAME) also i

25 ic NO synthase inhibitor NG-nito-L-arginine (L-NNA) and the neuronal NO synthase selective inhibitor

26 NO synthase inhibitor N(G)-nitro-L-arginine (L-NNA) co-treatment or scrambled C-peptide.

27 ynthase (NOS) inhibitor NG-nitro-l-arginine (L-NNA) corrected vascular tone defects in both assays.

28 e (DOCA)-salt and N(omega)-nitro-L-arginine (L-NNA) hypertensive but not normotensive rats develop sp

29 ide synthase inhibitor, NG-nitro-L-arginine (L-NNA) on free radical generation and myocardial contrac

30 NOS inhibitor N(G)-nitro-L-arginine (L-NNA) prevented the NO production.

31 synthase inhibitor Nomega-nitro-L-arginine (L-NNA) significantly blunted this response (mean vasodil

32 -arginine (L-NMMA) and N G-nitro L-arginine (L-NNA) to the superfusate abolished the positive correla

33 inhibition using N(omega)-nitro-L-arginine (L-NNA) was also assessed, because this combination has b

34 N(G)-nitro-L-arginine (L-NNA), an inhibitor of NO synthase (NOS), (5 mg/kg, i.p

35 hase (NOS) inhibitor N:(G)-nitro-L-arginine (L-NNA), and knockout mice carrying a homozygous targeted

36 lockade of NOS by N(omega)-nitro-L-arginine (L-NNA), but not by specific inducible (i)NOS or neuronal

37 ynthase inhibitor N(omega)-nitro-L-arginine (L-NNA), L-NNA plus L-citrulline, or L-arginine.

38 xide synthase inhibitor, N-nitro-L-arginine (L-NNA).

39 N(omega)-nitro-L-arginine (L-NNA, 10(-4) mol/L) significantly inhibited flow-induce

40 NO synthesis with N(omega)-nitro-L-arginine (L-NNA, 35 mg/kg IV).

41 N omega-nitro-L-arginine (L-NNA, NO synthase inhibitor) decreased Ik in sham rabbi

42 NO synthase inhibitor L-N(G)-nitro-arginine (L-NNA) and the guanylate cyclase inhibitor 1H-[1,2,4]oxa

43 for CO synthesis, N(omega)-nitro-L-arginine [L-NNA] for NO synthesis, and VIP(10-28) for VIP receptor

44 e (iNOS) inhibitor N(omega)-nitro-L-arginine(L-NNA) induced E-selectin expression at levels comparabl

45 h both L-NNA (1.97 +/- 0.35% increase before L-NNA, 0.00 +/- 0.02% during L-NNA) and TRIM (1.78 +/- 0

46 There was a significant correlation between L-NNA plasma AUC and the reduction in tumour blood volum

47 An interaction occurred between L-NNA induced vasomotion oscillations and the AFC respon

48 tion is inhibited during perfusion with both L-NNA (1.97 +/- 0.35% increase before L-NNA, 0.00 +/- 0.

49 muscles that were attenuated or abolished by L-NNA.

50 n W/W(V) muscles by EVS, and not affected by L-NNA.

51 P=0.01 versus NC), which was not affected by L-NNA.

52 Myocardial perfusion was not altered by L-NNA.

53 ary venous oxygen tension was not altered by L-NNA.

54 se defects, an effect markedly attenuated by L-NNA co-treatment.

55 cence by 0.76 +/- 0.09% which was blocked by L-NNA (change of 0.00 +/- 0.03%) but not TRIM (increase

56 he reversal of L-arginine-induced effects by L-NNA suggests that NO-NOS system may be playing a criti

57 , but this was not significantly modified by L-NNA.

58 enous oxygen tension was modestly reduced by L-NNA at all levels of myocardial oxygen consumption.

59 so-obliteration was significantly reduced by L-NNA treatment (43% decrease from controls).

60 ion of NANC nerve-mediated IAS relaxation by L-NNA was reversed by L-citrulline as well as L-arginine

61 increase before L-NNA, 0.00 +/- 0.02% during L-NNA) and TRIM (1.78 +/- 0.18% increase before TRIM, -0

62 activity and p110delta density in aorta from L-NNA and DOCA-salt rats.

63 Aortic homogenates from L-NNA rats also had elevated p110beta protein density, b

64 bited by the nitric oxide synthase inhibitor L-NNA.

65 ium channel blocker (TTX), an NOS inhibitor (L-NNA), or a specific inhibitor of neuronal NOS (7-NI).

66 was unchanged by the NO synthase inhibitor, L-NNA (10(-6) or 10(-3) M) (11+/-1 and 20+/-1 vs. 11+/-1

67 ntrast, the nitric oxide synthase inhibitor, L-NNA, and the protein kinase G inhibitor, Rp 8-Br cGMPs

68 from 163 micromol min(-1) L(-1) at 0.1 mg/kg L-NNA to 2150 micromol min(-1) L(-1) at 0.9 mg/kg L-NNA.

69 to 2150 micromol min(-1) L(-1) at 0.9 mg/kg L-NNA.

70 In the presence of 100 micromol/L L-NNA, 100 micromol/L atropine did not affect electrical

71 M L-NMMA (N(G)-monomethyl-L-arginine) + 1 mM L-NNA (N(G)-nitro-L-arginine) for 2-3 h plus inclusion o

72 r 2-3 h plus inclusion of 1 mM L-NMMA + 1 mM L-NNA in the patch pipette solution) produced no signifi

73 evated p110beta protein density, but neither L-NNA nor DOCA-salt had differences in p85alpha and p110

74 inhibitor N(omega)-nitro-L-arginine (L-NNA), L-NNA plus L-citrulline, or L-arginine.

75 Coadministration of L-NNA with iberiotoxin further decremented hypoxic pial

76 h tetrodotoxin (TTX) mimicked the effects of L-NNA on histamine responses.

77 L-Arginine prevented the effects of L-NNA.

78 Chronic injections of L-NNA alone did not modify either morphine antinocicepti

79 l field stimulation (EFS) in the presence of L-NNA and MRS 2500 enhanced ICC-IM Ca(2+) transients.

80 During local CTX + APA perifusion, L-NNA + INDO abolished SCVD while conducted [Ca2+]i resp

81 rfusion, but almost absent in dogs receiving L-NNA.

82 elivered selectively to the trachea in situ, L-NNA and ODQ also increased baseline cholinergic tone o

83 an inhibitor of nitric oxide (NO) synthesis, L-NNA, and an inhibitor of soluble guanylyl cyclase, ODQ

84 The L-NNA (4.8 mg/kg total) was infused intravenously during

85 arone and Ani9 inhibited the effects of TTX, L-NNA and ODQ.

86 er (GSK 7975 A) reversed the effects of TTX, L-NNA and ODQ.

87 Ca(2+) imaging revealed that TTX, L-NNA and ODQ increased Ca(2+) transient firing in colon

88 With L-NNA the Asc*- rose from 3.2 +/- 0.9 nmol/l to 4.0 +/-

89 With L-NNA, FAS declined from 36 +/- 13% (baseline) to 27 +/-

90 luorescence is reduced during perfusion with L-NNA and the increase in fluorescence during high frequ