ライフサイエンスコーパス: nitroarginine

1 sed the NOS inhibitors 7-nitroindazole and L-nitroarginine.

2 ncrease in renal efflux of 20-HETE, as did L-nitroarginine.

3 ium or the nitric-oxide synthase inhibitor L-nitroarginine.

4 revented by the nonselective NOS inhibitor L-nitroarginine (3 mmol/L) or the specific iNOS inhibitor

5 By contrast, oral administration of L-nitroarginine (an exogenous antagonist of NO synthase) r

6 a library of 152 dipeptide amides containing nitroarginine and amino acids other than Phe are synthes

7 L-N(omega)-nitroarginine and L-arginine were coupled with N-(Cbz-al

8 arteries pretreated with indomethacin and L-nitroarginine and preconstricted with U46619, 14,15-EEZE

9 ynthase inhibitors NG-monomethyl-L-arginine, nitroarginine, and aminoguanidine.

10 A series of N omega-nitroarginine (ArgNO2)- and phenylalanine-containing dip

11 A series of L-nitroarginine-based dipeptide inhibitors are highly sele

12 These included Ngamma-methylarginine, Ngamma-nitroarginine, citrulline, homoarginine, and three confo

13 We previously reported nitroarginine-containing dipeptide amides and some pepti

14 Recently, we reported nitroarginine-containing dipeptide amides and some pepti

15 The D-nitroarginine-containing dipeptide inhibitors are not di

16 ection for nNOS over eNOS observed for the L-nitroarginine-containing dipeptide inhibitors reported p

17 Starting with the nitroarginine-containing dipeptide inhibitors we develop

18 e nNOS and eNOS heme domain bound with two D-nitroarginine-containing dipeptide inhibitors, D-Lys-D-A

19 ight be the structural basis for why these D-nitroarginine-containing inhibitors are selective for nN

20 ions of NOS that also received injections of nitroarginine; cortical barrels formed normally in these

21 ss, blockade of NOS with daily injections of nitroarginine from P14 to P56 fails to prevent the forma

22 d by whisker ablation at birth was normal in nitroarginine-injected NOS knock-out mice.

23 autoradiography in rats treated daily with l-nitroarginine (l-NA) following neonatal unilateral vibri

24 Second, L-nitroarginine (L-NA), an NOS inhibitor, increases the ra

25 tol tetranitrate (PETN), the NOS inhibitor l-nitroarginine (L-NA), plasma pool C1-INH, and the B2R an

26 nimals, while its less-active stereoisomer D-nitroarginine methyl ester (D-NAME, 200 microM) had no s

27 eraction is blocked by eNOS inhibitor L-N(G)-nitroarginine methyl ester (hydrochloride) and Src kinas

28 (n=18, with n=15 controls) induced by l-N(G)-nitroarginine methyl ester (L-NAME) and pressure overloa

29 ologic inhibition of NO synthase with L-N(G)-nitroarginine methyl ester (L-NAME) and stimulation of g

30 ic oxide synthase (NOS) inhibitor L-N(omega)-Nitroarginine methyl ester (L-NAME) and the anti-oxidant

31 blocked by the NO synthase inhibitor L-N(G)-nitroarginine methyl ester (L-NAME) but not by D-NAME.

32 reated with the NO synthase inhibitor L-N(G)-nitroarginine methyl ester (L-NAME) from gestational day

33 ed their relationship in vivo using the L-NG-Nitroarginine Methyl Ester (L-NAME) induced PE-like rat

34 L-NG-nitroarginine methyl ester (L-NAME), but not D-NG-nitroa

35 in nNOS(-/-) mice and reduced by L-N(omega)-nitroarginine methyl ester (L-NAME), indicating uncoupli

36 platelets with the NO synthase inhibitor -NG-nitroarginine methyl ester (L-NAME), reduced NO producti

37 ically treated with the NOS inhibitor l-N(G)-nitroarginine methyl ester (L-NAME).

38 an effect not reversed by the NO inhibitor L-nitroarginine methyl ester (L-NAME).

39 icroM) and a competitive inhibitor of NOS, L-nitroarginine methyl ester (L-NAME, 200 microM), signifi

40 se (to scavenge superoxide anions) or L-N(G)-nitroarginine methyl ester (L-NAME, a nonselective nitri

41 f inhibitors of nitric oxide synthesis (L-NG-nitroarginine methyl ester [L-NAME]) or protein nitrosyl

42 rvated Rana tadpole optic tecta using L-N(G)-nitroarginine methyl ester in Elvax.

43 The NOS inhibitor L-nitroarginine methyl ester is neuroprotective in wild-ty

44 nsin type 1 blockade reduces injury in the l-nitroarginine methyl ester model but increases tissue in

45 itial nitric oxide synthase inhibitor l-N(6)-nitroarginine methyl ester or bradykinin B2 receptor ant

46 kage of NOS activity with the inhibitor L-NG-nitroarginine methyl ester or genetic eNOS deficiency ab

47 eutrophil interactions, or those receiving L-nitroarginine methyl ester to inhibit nitric oxide synth

48 esponse was unaffected by indomethacin, l-NG-nitroarginine methyl ester, a bradykinin B2 receptor ant

49 course if VEGF was co-incubated with L-N(G)-nitroarginine methyl ester, a competitive eNOS inhibitor

50 erimental hypertension (angiotensin II, L-NG-nitroarginine methyl ester, and high salt).

51 or antagonist MK-801 and the NOS inhibitor L-nitroarginine methyl ester, but not its inactive stereoi

52 with the nitric oxide synthase inhibitor, L-nitroarginine methyl ester, formation of both nitric oxi

53 arginine methyl ester (L-NAME), but not D-NG-nitroarginine methyl ester, increased high SS-induced EM

54 ene-glycolated superoxide dismutase (SOD), l-nitroarginine methyl ester, or sepiapterin not only reve

55 The competitive NO synthase inhibitor, L-nitroarginine methyl ester, prevents Ras activation elic

56 nd BMP4 was inhibited by the NOS inhibitor l-nitroarginine methyl ester, providing functional evidenc

57 BMDEC migration that was inhibited by L-N(G)-nitroarginine methyl ester.

58 n with H89 and NO synthase inhibition with l-nitroarginine methyl ester.

59 y an inhibitor of nitric-oxide synthetase, L-nitroarginine methyl ester.

60 l ester, but not its inactive stereoisomer D-nitroarginine methyl ester.

61 15-LOX(-/-) aortic rings in the absence of L-nitroarginine-methyl ester, and ang II impaired acetylch

62 was a twofold increase in the magnitude of l-nitroarginine-methyl ester-inhibitable, acetylcholine-de

63 bin or the nitric oxide synthase inhibitor L-nitroarginine methylester.

64 he lack of a free alpha-amino group on the D-nitroarginine moiety makes the dipeptide inhibitor steer

65 two inhibitors of nitric oxide synthase (NG-nitroarginine [NNA] or aminoguanidine).

66 idonic acid and indomethacin-resistant and L-nitroarginine-resistant relaxations to bradykinin.

67 transfer through heme (7-nitroindazole and N-nitroarginine) stimulated the rate to a small extent.