ライフサイエンスコーパス: ET(A) receptor antagonist

1 f two moderately potent series of nonpeptide ETA receptor antagonists.

2 ides are potent and selective small molecule ETA receptor antagonists.

3 d this increase was blocked with a selective ET(A) receptor antagonist.

4 H compound of our series of novel synthetic (ET(A)) receptor antagonists.

5 n, either saline (negative control), BQ-123 (ETA receptor antagonist, 10 microg/min), BQ-788 (ETB rec

6 The ET(A) receptor antagonist (2) (N-(3,4-dimethyl-5-isoxazo

7 structural elements in a biphenylsulfonamide ET(A) receptor antagonist (2) followed by additional opt

8 ET-1 (2 and 6 pmol/min); BQ-123, a selective ET(A) receptor antagonist (3 and 10 nmol/min); and BQ-78

9 Therefore, although the ETA receptor antagonist A-127722 can inhibit ETA-mediate

10 rteries of DOCA-salt rats with the selective ETA receptor antagonist ABT-627, NADPH oxidase inhibitor

11 ting our hypothesis that the combined use of ET(A) receptor antagonist (ABT-627; Atrasentan) with Tax

12 d DOCA-salt rats was reversed by a selective ET(A) receptor antagonist, ABT-627, the flavoprotein inh

13 e studied the effects of BQ 123, a selective ET(A) receptor antagonist, after ligation of the ductus

14 with longer duration than DARA 3 or AT(1) or ET(A) receptor antagonists alone.

15 Furthermore, the selective ET(A) receptor antagonist ambrisentan attenuated the inc

16 In the outer medulla, both the ET(A) receptor antagonist and triple therapy reduced the

17 intravitreous injections of ET-1; BQ-123, an ETA receptor antagonist; and phosporamindon, an endothel

18 ]-2-sulfonamide derivatives as endothelin-A (ET(A)) receptor antagonists are described.

19 mized in a double-blind manner to either the ET(A) receptor antagonist atrasentan (10 mg) or placebo

20 oto-Kakizaki (GK) rats treated with vehicle, ET(A) receptor antagonist atrasentan (5 mg x kg(-1) x da

21 vels and that pretreatment with PD156707, an ETA receptor antagonist, blocks the rebound hypertension

22 er a 60-minute intracoronary infusion of the ET(A) receptor antagonist BQ-123.

23 vious exposure of cells to the endothelin-A (ET(A)) receptor antagonist BQ-123 (1 microm) prevented E

24 .001), whereas infusion of the endothelin-A (ET(A)) receptor antagonist BQ-123 significantly reduced

25 ium nitroprusside and the endothelin type A (ET(A)) receptor antagonist BQ-123 were assessed using ve

26 Cotreatment with the ETA receptor antagonist BQ 610 prevented these effects,

27 ne study, six subjects received placebo, the ETA receptor antagonist BQ-123 alone, and BQ-123 in comb

28 (-1)) was administered in the presence of an ET(A) receptor antagonist, BQ-123 (1 mg/kg).

29 was strongly inhibited by the endothelin-A (ET(A)) receptor antagonist, BQ-123 (3.2 m).

30 gonist, BQ-788, but not by the endothelin A (ET(A)) receptor antagonist, BQ-123, consistent with pred

31 ET-1-induced responses were inhibited by the ET(A) receptor antagonist BQ123 and the phospholipase C

32 ET(A) receptor antagonist BQ123 inhibited most (approxim

33 ET1 effects on [Ca2+]i were prevented by the ETA receptor antagonist BQ123 (cyclo-D-Asp-Pro-D-Val-Leu

34 emia, we determined the effect of a specific ET(A) receptor antagonist, BQ123 (1mg/kg, intravenously

35 The specific ET(A) receptor antagonist, BQ123, significantly inhibite

36 A specific ET(A) receptor antagonist, BQ123, was infused (40 nmol/m

37 present study, we investigated the effect of ET(A) receptor antagonists, BQ123 and BMS182874, on morp

38 Effect of ETA-receptor antagonist, BQ123, on postischemic hypoperf

39 bation of coronary segments with a selective ETA receptor antagonist, BQ485 (1 mumol/L), had no effec

40 Et-1-induced IL-8 production was blocked by ET(A) receptor antagonist BQ610, but not by ET(B) recept

41 through ET(A) receptors, because a specific ET(A) receptor antagonist (BQ610) blocked these effects

42 by ET-1 was prevented by BQ-123, a selective ET(A) receptor antagonist, but was not affected by pertu

43 BQ-123, an ETA receptor antagonist, but not saralasin, an angiotens

44 Therefore, ET(A) receptor antagonists did not bind directly to opio

45 very of a potent and selective endothelin A (ETA) receptor antagonist for the potential treatment of

46 e Ad.ET-1 group, intravenous infusion of the ET(A) receptor antagonist FR 139317 reduced the blood pr

47 ion is therefore amenable to reversal by the ET(A) receptor antagonist FR139317, and this model may o

48 The endothelin-A (ET(A)) receptor antagonist FR139317 (3 or 30 nmol) injec

49 ith the infusion of either the endothelin-A (ETA) receptor antagonist FR139317, or saline vehicle.

50 Mice treated concomitantly with the ET(A) receptor antagonist had lower BP and fewer CD3(+)

51 at long-term treatment with an endothelin-A (ET(A)) receptor antagonist improves coronary endothelial

52 odynamic effects of sitaxsentan, a selective ET(A) receptor antagonist, in patients with chronic stab

53 tral endopeptidase inhibitor) and BQ-123 (an ETA receptor antagonist) increased FBF by 52 +/- 10% (P

54 ECE inhibitors and ETA receptor antagonists may be useful as vasodilator ag

55 ETA receptor antagonists may prevent rebound pulmonary h

56 We have previously disclosed the selective ET(A) receptor antagonist N-(3,4-dimethyl-5-isoxazolyl)-

57 during HPP (n=7), isch kidneys receiving the ETA receptor antagonist (n=7), and isch kidneys receivin

58 line, AngII infusion, AngII infusion with an ET(A) receptor antagonist, or AngII infusion with triple

59 y vasoconstriction, which was blocked by the ETA receptor antagonist PD 156707 (n=3).

60 concomitant administration of the selective ETA receptor antagonist (PD 156707 24 mg/d), and sham co

61 These findings indicate that ET(A) receptor antagonists potentiate morphine antinocic

62 roteinuric CKD to compare the effects of the ET(A) receptor antagonist sitaxentan, nifedipine, and pl

63 n patients with HF, we infused the selective ET(A) receptor antagonist sitaxsentan at increasing rate

64 In a preliminary PAH study, the selective ET(A) receptor antagonist sitaxsentan improved six-min w

65 Treatment with the selective ET(A) receptor antagonist sitaxsentan, orally once daily

66 optimal dose of the selective endothelin A (ET(A)) receptor antagonist sitaxsentan for the treatment

67 osure to either BQ123 (10 microM), selective ETA receptor antagonist, U73122 (5 microM), or SKF 96365

68 ocked effects of ET-1 and sarafotoxin 6c; an ET(A) receptor antagonist was without effect.

69 dy, we show that HJP-272, a highly selective ET(A) receptor antagonist with an IC(50) of 70.1 nmol/L,

70 Mechanism of interaction of ET(A) receptor antagonists with morphine was investigate