ライフサイエンスコーパス: BQ-123

1 educed hemoglobin could not be attenuated by BQ-123.

2 reduction was prevented by pretreatment with BQ-123.

3 ry infusion of the ET(A) receptor antagonist BQ-123.

4 between any risk factor and the response to BQ-123.

5 inutes) was inhibited (P < 0.03) by 10(-4) M BQ-123.

6 BQ-123 (0.4 mg/h) was used to block the endothelin-1 (ET

7 BQ-123 increased effective renal blood flow (BQ-123, -0.1 +/- 2.4%; BQ-123+E, 10.9 +/- 4.2%; P < 0.01

8 at surgery, and treated animals with either BQ 123 (1 mg/d) or vehicle (0.1% DMSO, HTN) in the pulmo

9 he presence of an ET(A) receptor antagonist, BQ-123 (1 mg/kg).

10 the endothelin-A (ET(A)) receptor antagonist BQ-123 (1 microm) prevented ET-1-induced shifts in TTX-R

11 onstriction (-2.0+/-1.1%) was reversed after BQ-123 (+1.0+/-0.7%), especially in dysfunctional segmen

12 ncy: cyclo(L-Pro-D-Val-L-Leu-D-Trp-D-Asp) or BQ-123 = 1.0, cyclo(L-Pro-D-Pro-L-Leu-D-Trp-D-Asp) = 0.0

13 reduced effective renal vascular resistance (BQ-123, -1.2 +/- 3.1%; BQ-123+E, -12.8 +/- 3.0%; P < 0.0

14 (30 nmol/min), the endothelin ETA antagonist BQ-123 (100 nmol/min), and both combined.

15 increased urinary sodium excretion markedly (BQ-123, 2.6 +/- 12.8%; BQ-123+E, 25.2 +/- 12.6%; P < 0.0

16 E inhibition (mean area under curve +/- SEM; BQ-123, -2.3 +/- 1.8%; BQ-123+E, -5.1 +/- 1.1%; P < 0.05

17 Vs represented by the mean luminal stenosis (BQ-123=29+/-13% and sarafotoxin S6c=27+/-11% reduction,

18 thelin-1 (1-20 nmol), alone or together with BQ-123 (3.2 m), into the plantar hindpaw receptive field

19 he endothelin-A (ET(A)) receptor antagonist, BQ-123 (3.2 m).

20 roma reduced hemoglobin in rats treated with BQ-123 (5 mg/kg/hr iv) increased the blood pressure to a

21 duced) hemoglobin in control (untreated) and BQ-123 (5 mg/kg/hr iv)-treated rats.

22 t this hypothesis, we studied the effects of BQ 123, a selective ET(A) receptor antagonist, after lig

23 artery infusions of ET-1 (2 and 6 pmol/min); BQ-123, a selective ET(A) receptor antagonist (3 and 10

24 I 3-kinase activity by ET-1 was prevented by BQ-123, a selective ET(A) receptor antagonist, but was n

25 Second, BQ-123, a selective ET(A)R antagonist, abolished the res

26 In contrast, BQ-123 administration resulted in a significant vasodila

27 ; however, in hypercholesterolemic patients, BQ-123 administration resulted in a significant vasodila

28 asodilatation (32+/-1%, P=0.0001) similar to BQ-123 alone (P=0.98).

29 Treatment with BQ-123 alone on day 1 did not affect the dilation to ilo

30 eceived placebo, the ETA receptor antagonist BQ-123 alone, and BQ-123 in combination with the ETB rec

31 inal fluid (aCSF); (2) autologous blood; (3) BQ-123 alone; or (4) BQ-123 in combination with blood.

32 Treatment with BQ-123 along with hematoma blocked the reduction in cAMP

33 Treating piglets with BQ-123 along with hematoma on day 1 prevented the hemato

34 ECE and neutral endopeptidase inhibitor) and BQ-123 (an ETA receptor antagonist) increased FBF by 52

35 mooth coronary arteries (normal), we infused BQ-123, an antagonist of the ET(A) receptor, into a majo

36 Mean arterial pressure was reduced by BQ-123, an effect that was doubled during ACE inhibition

37 -788, an ET receptor B (ETB) antagonist; and BQ-123, an ET receptor A (ETA) antagonist.

38 BQ-123, an ETA receptor antagonist, but not saralasin, a

39 ated after intravitreous injections of ET-1; BQ-123, an ETA receptor antagonist; and phosporamindon,

40 esterolemic patients received co-infusion of BQ- 123 and BQ-788 (a selective blocker of ETB receptors

41 In modified Langendorff perfusions, ERAs (BQ-123 and bosentan 10(-7,-6,-5) mol/L) decreased contra

42 atients with diabetes received coinfusion of BQ-123 and BQ-788 (a selective blocker of ET(B) receptor

43 blockade of ET-1 receptors by co-infusion of BQ-123 and BQ-788 (P=0.66).

44 of ET-1 receptors obtained by coinfusion of BQ-123 and BQ-788.

45 of ET-1 receptors obtained by co-infusion of BQ-123 and BQ-788.

46 or ET(B) receptor antagonists, respectively BQ-123 and BQ788, when administered separately.

47 Both BQ-123 and sarafotoxin S6c significantly reduced CFVs re

48 e skin blood flow (SkBF) during graded ET-A (BQ-123) and ET-B (BQ-788) antagonist infusions in women

49 n of a selective blocker of ET(A) receptors (BQ-123) and, on a different occasion, to ET-1, were meas

50 ion of a selective blocker of ETA receptors (BQ-123) and, on a separate occasion, to ET-1 were measur

51 +/- 3.0%; P < 0.01 versus placebo and versus BQ-123), and increased urinary sodium excretion markedly

52 y with an ETA receptor-selective antagonist, BQ-123, and an inhibitor of ET-converting enzyme (ECE),

53 who were pretreated with E received placebo, BQ-123, and BQ-123 with concomitant inhibition of nitric

54 holine, substance P, sodium nitroprusside or BQ-123 between patients and control subjects.

55 p did not alter the high-affinity binding of BQ-123, bosentan, or SB 209670.

56 In addition, BQ-123 caused a significant increase in the diameter of

57 orearm vasoconstriction (13+/-1%, P=0.0001); BQ-123 caused local vasodilatation (33+/-3%, P=0.0001).

58 significant vasoconstriction (P < .001) and BQ-123 caused significant vasodilatation (P < .001).

59 Combined thiorphan and BQ-123 caused vasodilatation (32+/-1%, P=0.0001) similar

60 he endothelin A (ET(A)) receptor antagonist, BQ-123, consistent with predominant ET(B) receptor expre

61 The endothelin-A receptor antagonist, BQ-123, could attenuate the systemic hemodynamic and reg

62 BQ-123 did not affect FBF in normotensive subjects (P=0.

63 In normal subjects, BQ-123 did not significantly modify FBF from baseline (P

64 In normal subjects, BQ-123 did not significantly modify FBF from baseline (p

65 ic inhibitor of A-type endothelin receptors (BQ-123) did not (-2.0+/-0.2 pmol mm(-1) min(-1), P = NS

66 BQ-123 dilated the coronary circulation; D increased by

67 vascular resistance (BQ-123, -1.2 +/- 3.1%; BQ-123+E, -12.8 +/- 3.0%; P < 0.01 versus placebo and ve

68 under curve +/- SEM; BQ-123, -2.3 +/- 1.8%; BQ-123+E, -5.1 +/- 1.1%; P < 0.05 versus placebo).

69 ive renal blood flow (BQ-123, -0.1 +/- 2.4%; BQ-123+E, 10.9 +/- 4.2%; P < 0.01 versus BQ-123), reduce

70 m excretion markedly (BQ-123, 2.6 +/- 12.8%; BQ-123+E, 25.2 +/- 12.6%; P < 0.05 versus BQ-123, P < 0.

71 and ET(B) receptors by combined infusion of BQ-123 (ET(A) blocker; 100 nmol/min) and BQ-788 (ET(B) b

72 infusion, either saline (negative control), BQ-123 (ETA receptor antagonist, 10 microg/min), BQ-788

73 Lambs treated with BQ 123 had lower PVR after delivery during ventilation w

74 crease was completely blocked by losartan or BQ-123, implying a role for angiotensin and endothelin a

75 e selective endothelin receptor A antagonist BQ-123 in a dose-dependent manner.

76 The augmented vasodilatation to BQ-123 in cirrhotic patients is consistent with a compen

77 ) autologous blood; (3) BQ-123 alone; or (4) BQ-123 in combination with blood.

78 he ETA receptor antagonist BQ-123 alone, and BQ-123 in combination with the ETB receptor antagonist B

79 BQ-123 increased effective renal blood flow (BQ-123, -0.

80 ese subjects, antagonism of ETA receptors by BQ-123 increased forearm flow during saline (P < 0.001)

81 BQ-123 induced significant dilation in the normal arteri

82 pmol mm(-1) min(-1), P < 0.03), but that for BQ-123-infused (NH4)2SO4 animals was not (42.9+/-4.2 pmo

83 After BQ-123 infusion, exogenously infused ET-1 did not signif

84 flow changes comparable to those measured in BQ-123 injected diabetic rats.

85 measured after ETA receptor antagonism with BQ-123 injection.

86 provement in D and CVR responses to ACH with BQ-123 inversely correlated with baseline ACH responses

87 The endothelin Type A receptor antagonist BQ 123 lowered the high portal resistance in BDL rats to

88 When ET-1 was given after BQ-123, no significant drop in TMV was noted.

89 We examined effects of the ET-1 antagonist, BQ-123, on hematoma-induced modification of pial arterio

90 ated with either vehicle or EDNRA antagonist BQ-123 or EDNRB antagonist BQ-788 on P12, and kept at ro

91 Importantly, infusion of BQ-123 or ET-1 distal to the common iliac artery did not

92 he endothelin-A (ET(A)) receptor with either BQ-123 or with HJP-272, the 6-OH compound of our series

93 ith an aerosolized ET-A receptor antagonist (BQ-123) or an ET-B receptor antagonist (BQ-788) before e

94 In contrast, coincubation with ET(A) (BQ-123) or ET(B) (BQ-788) receptor antagonists had no ef

95 a recently optimized endothelin antagonist, BQ-123, originally isolated from microbial sources by Ba

96 itially dilated with ACH did not change with BQ-123 (P=NS).

97 ith 10% O2, 100% O2, and inhaled NO (HTN vs. BQ 123, P < 0.05 for each intervention).

98 + septum (0.79+/-0.03, HTN vs. 0.57+/-0.06, BQ 123, P < 0.05) and attenuated the increase in wall th

99 pulmonary arteries (61+/-2, HTN vs. 50+/-2%, BQ 123, P < 0.05).

100 iosus ligation (78+/-2, HTN vs. 70+/-4 mmHg, BQ 123, P < 0.05).

101 %; BQ-123+E, 25.2 +/- 12.6%; P < 0.05 versus BQ-123, P < 0.01 versus placebo and versus E) only durin

102 ic injection of the ET-A receptor antagonist BQ-123 partially blocked tumor-associated mechanical hyp

103 ET-1, which was abrogated by BQ-788, but not BQ-123, pretreatment, suggesting functional coupling of

104 ls, and the subsequent injection of 10(-4) M BQ-123 produced retinal blood flow changes comparable to

105 4%; BQ-123+E, 10.9 +/- 4.2%; P < 0.01 versus BQ-123), reduced effective renal vascular resistance (BQ

106 enuated ET-1 responses (P < .001), augmented BQ-123 responses (P < .001), and similar BQ-788 response

107 variable positions uniquely rediscovered the BQ-123 sequence or cyclo(L-Pro-D-Val-L-Leu-D-Trp-D-Asp).

108 the endothelin-A (ET(A)) receptor antagonist BQ-123 significantly reduced PWV by 12 +/- 4% (p < 0.001

109 Besides being resistant to BQ-123, the maximal response in diabetic animals occurre

110 ities of the constrained cyclic pentapeptide BQ-123, the pyrimidinylbenzenesulfonamide bosentan, the

111 to the kidney and musculoskeletal system of BQ-123-treated rats as compared with control rats.

112 ys and liver was significantly attenuated in BQ-123-treated rats as compared with control rats.

113 ked hemoglobin were significantly blocked in BQ-123-treated rats as compared with control rats.

114 ked hemoglobin were significantly blocked in BQ-123-treated rats as compared with control rats.

115 duced increase in blood flow to the heart of BQ-123-treated rats was similar to the increase in contr

116 Acute BQ 123 treatment (2 mg/30 min) lowered PVR in three HTN

117 Chronic BQ 123 treatment attenuated the rise in mean pulmonary a

118 Chronic BQ 123 treatment prevented the development of RVH as det

119 BQ-123 treatment along with hematoma prevented both the

120 BQ-123 treatment significantly reduced these alterations

121 ponse in rats (n = 9) injected with 10(-4) M BQ-123 was significantly (P < 0.001) blunted compared to

122 In normotensives, FBF response to BQ-123 was similar in white (n =22) and black (n =15) pa

123 ndothelin type A (ET(A)) receptor antagonist BQ-123 were assessed using venous occlusion plethysmogra

124 Although no analogs more potent than BQ-123 were discovered, our results provide verification

125 erial infusion of an ET(A) receptor blocker (BQ-123) were analyzed by plethysmography in 37 normotens

126 BQ-123, when coinjected with ET-1, blocked ET-1-induced

127 try; the angiotensin response was blocked by BQ-123, whereas the endothelin response was unaffected b

128 us difference in ET-1 levels developed after BQ-123, which was consistent with enhanced cardiac clear

129 treated with E received placebo, BQ-123, and BQ-123 with concomitant inhibition of nitric oxide (NO)

130 o coronary tone, we compared the dilation to BQ-123 with that elicited by intracoronary nitroglycerin