ライフサイエンスコーパス: HOE 140

1 al with a bradykinin B2 receptor antagonist (HOE 140).

2 ization) were blocked by the B(2) antagonist HOE 140.

3 140 but not by the B(2) receptor antagonist HOE 140.

4 nction of losartan was completely blocked by HOE 140.

5 h losartan, whereas the reverse was true for HOE 140.

6 vated the receptor; this also was blocked by HOE 140.

7 likrein were blocked by the B(2) antagonist, HOE 140.

8 ; this effect was blocked by the antagonist, HOE 140.

9 h were blocked by the B2-receptor antagonist HOE 140.

10 inomycin D and the B2 BK receptor antagonist HOE-140.

11 ed by the effect of single changes in BK and HOE-140.

12 the structurally related peptide antagonist HOE-140.

13 renal function was studied before and after Hoe 140 (0.1 mg s.c. and i.v.) or vehicle.

14 (-1), P=0.002); this effect was abolished by HOE 140 (0.1+/-0.3 ng x min(-1) x 100 mL(-1), P=0.036 ve

15 ypertension in rats treated with vehicle and Hoe-140 (0.1 microM).

16 Blocking endogenous bradykinin with HOE-140 (0.3 mg/kg), a specific bradykinin B2-receptor a

17 The bradykinin (BK) antagonists HOE 140 (1 mg kg-1, i.v.) did not affect the response in

18 The bradykinin (BK) antagonist HOE 140 (1 mg kg-1, i.v.) did not affect the response in

19 hed by the bradykinin B2 receptor antagonist HOE 140 (1 microM).

20 ent with the selective bradykinin antagonist HOE 140 (10 micromol/L) attenuated ramiprilat-induced in

21 presence of losartan (4.5 micromol/L) and/or HOE 140 (10 micromol/L).

22 nt were blocked by a B2 receptor antagonist (HOE-140; 10 microm) or a protein kinase C (PKC) inhibito

23 etreated with bradykinin receptor antagonist HOE 140 (100 microg/kg intravenously) or vehicle.

24 absence of (1) the B(2) receptor antagonist HOE 140 (100 microg/kg IV), (2) the NO synthase inhibito

25 ,Hyp(3),Thi(5),D-Tic(7), Oic(8)]-bradykinin (HOE 140, 5x10(-8) mol/l) significantly reduced the effec

26 rn rats with the selective BK-B2 antagonist, Hoe 140 (600 micrograms/kg per day, sc), from days 1 thr

27 efore and after an intrabrachial infusion of Hoe-140 (a potent, selective, and long-acting bradykinin

28 Hoe 140, a bradykinin B2-receptor antagonist, had no eff

29 The bradykinin B2 receptor antagonist HOE 140 abolished the protective effect of preconditioni

30 In agreement, HOE-140 affected in the same way expression levels of ne

31 000- and 150-fold, respectively, while [Ala9]HOE-140 affinity is reduced 7-fold and [Ala6]HOE-140 aff

32 In contrast, HOE-140 affinity is reduced less than 7-fold by F254A, F

33 HOE-140 affinity is reduced 7-fold and [Ala6]HOE-140 affinity is unchanged.

34 sed, indicating depressed contractility with HOE-140 after CHF.

35 HOE-140 also abolished the increase in plasminogen activ

36 The B2 bradykinin receptor antagonist HOE 140 and the B1 bradykinin receptor antagonist des-Ar

37 The binding of HOE-140 and the binding of bradykinin are mutually exclu

38 N(omega)-Nitro-L-arginine methyl ester, HOE-140, and dichloroisocoumarin essentially abolished t

39 e of mutations that affect BK binding versus HOE-140 binding is surprising, but it was paralleled by

40 Models of HOE-140 binding to the receptor place its beta-turn one

41 HOE 140 blocked these effects.

42 ctant protein 1 (MCP-1) peaked postdialysis; HOE-140 blunted the increase in MCP-1 (5.9 +/- 5.9 versu

43 d by the B(1) receptor antagonist des-arg(10)HOE 140 but not by the B(2) receptor antagonist HOE 140.

44 during enalaprilat compared with vehicle or HOE 140, but not compared with baseline, and the effect

45 ked by the bradykinin B2 receptor antagonist HOE 140, by inhibition of the Ca2+-independent phospholi

46 Hoe 140 consistently blocked the vasodepressor action of

47 radykinin B2 receptor antagonist [Pro3, Phe5]HOE 140 (D-Arg0-Arg1-Pro2-Pro3-Gly4-Phe5-Ser6-D-Tic7+ ++

48 2A tested was the newer compound, icatibant (Hoe 140; D-Arg,[Hyp3,Thi5,D-Tic7,Oic8]-bradykinin).

49 Hoe 140 did not affect renal function in control rats, b

50 Chronic treatment with HOE-140 diminished eNOS and nNOS as well as M1-M4 muscar

51 In the presence of the B2BkR antagonist HOE-140 during rat neurosphere differentiation, neuron-s

52 Following administration of HOE 140, functional hyperaemia in the soleus muscle was

53 Following administration of HOE 140, functional hyperaemia in the soleus muscle was

54 Despite this, Hoe-140 had no discernible effects after enalapril or lo

55 inhibitors and a single bolus of icatibant (HOE-140) immediately before anesthesia (angiotensin-conv

56 sults document that losartan reduced whereas HOE 140 increased myocardial ischemia/reperfusion injury

57 nal mechanism for neural fate determination, HOE-140 induced up-regulation of Notch1 and Stat3 gene e

58 tive antagonists for BK, PAF, and histamine (Hoe-140: Ki = 10.1 to 11.9 nM; PCA-4248: Ki = 315 to 421

59 Neither Hoe 140 nor Nomega-nitro--arginine methyl ester, a nitri

60 There was no specific effect of HOE 140 on FBF or forearm vascular resistance (FVR, 29.9

61 There was no effect of enalaprilat or HOE 140 on the FBF or t-PA response to methacholine.

62 tan, and a bradykinin B(2) receptor blocker, HOE 140, on myocardial protection.

63 cal administration of either B1 (des-Arg(10)-Hoe-140) or B2 (Hoe-140) receptor antagonists.

64 re significantly attenuated by NPC 17647 and Hoe 140 (p < 0.05), two bradykinin B2 receptor antagonis

65 Incremental doses of B9340, but not HOE-140, produced a dose-dependent vasoconstriction (P=0

66 on of either B1 (des-Arg(10)-Hoe-140) or B2 (Hoe-140) receptor antagonists.

67 Blocking endogenous bradykinin with HOE-140 reduced coronary blood flow and produced signifi

68 receptor-specific antagonists (atropine and HOE 140, respectively).

69 -1) x min(-1) x 100 mL(-1) after vehicle and HOE 140, respectively, P=0.956 between groups).

70 copy of all of the peptidic analogs of BK or HOE-140 revealed a beta-turn at the C terminus.

71 In contrast, HOE-140 significantly accentuated the effect of dialysis

72 Similarly, this was despite the finding that Hoe-140 significantly reduced vasodilatation to bradykin

73 Hoe 140 treatment had no effect on kidney protein or RNA

74 In contrast to Hoe 140 treatment, neonatal protein undernutrition resul

75 inin-receptor antagonist, icatibant acetate (HOE 140), was used to determine the contribution of brad

76 The effects were also blocked by HOE 140, which blocks the bradykinin B2-kinin receptor,

77 Bk was blocked by the B2 receptor antagonist HOE-140, which indicates that the response was due to ac

78 fect of the bradykinin B(2) receptor blocker HOE-140 with vehicle on markers of oxidative stress, inf