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 i.v. iron and by the ET receptor antagonist BQ-123.

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

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

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

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

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

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

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

13 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

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

15 (30 nmol/min), the endothelin ETA antagonist BQ-123 (100 nmol/min), and both combined.

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

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

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

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

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

21 r between conditions (80% saline: 25 +/- 10, BQ-123: 30 +/- 7 mmHg; P = 0.17).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

39 -788, an ET receptor B (ETB) antagonist; and BQ-123, an ET receptor A (ETA) antagonist.

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

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

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

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

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

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

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

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

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

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

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

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

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

53 +/- 3.0%; P < 0.01 versus placebo and versus BQ-123), and increased urinary sodium excretion markedly

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

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

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

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

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

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

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

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

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

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

64 ntensities (80% saline: Delta3818+/-1222 vs. BQ-123: Delta4812+/-1469 ml/min; P = 0.001).

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

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

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

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

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

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

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

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

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

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

75 tudied during exercise with either saline or BQ-123 (ET(A) receptor antagonist) infusion following a

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

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

78 n vitro after treatment with as little as 10 Bq [(123)I]CC1.

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

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

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

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

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

84 BQ-123 increased blood flow at rest (79 +/- 87 ml/min; P

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

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

87 BQ-123 induced significant dilation in the normal arteri

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

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

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

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

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

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

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

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

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

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

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

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

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

101 ion blockade with the endothelin-1 inhibitor BQ-123, or ROS scavenging after SDRT using peroxiredoxin

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

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

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

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

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

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

108 %; BQ-123+E, 25.2 +/- 12.6%; P < 0.05 versus BQ-123, P < 0.01 versus placebo and versus E) only durin

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

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

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

112 BQ-123 reduced leg MAP at rest (-8 +/- 4 mmHg; P < 0.001

113 4%; BQ-123+E, 10.9 +/- 4.2%; P < 0.01 versus BQ-123), reduced effective renal vascular resistance (BQ

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

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

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

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

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

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

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

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

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

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

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

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

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

127 BQ-123 treatment along with hematoma prevented both the

128 BQ-123 treatment significantly reduced these alterations

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

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

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

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

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

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

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

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

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

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