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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

50 Myocardial perfusion was not altered by L-NNA.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

66 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.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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