ライフサイエンスコーパス: ET(B) receptor

1 f BQ- 123 and BQ-788 (a selective blocker of ETB receptors).

2 of BQ-123 and BQ-788 (a selective blocker of ET(B) receptors).

3 selectivity for the ETA receptor versus the ETB receptor.

4 greater than 1000-fold selectivity over the ETB receptor.

5 , by a mechanism dependent upon both ETA and ETB receptors.

6 ulature, in contrast to a slight increase in ETB receptors.

7 crovascular endothelial cells overexpressing ETB receptors.

8 ssion, which increases NHE3 activity via the ET(B) receptor.

9 dilation, which with ET-1 should involve the ET(B) receptor.

10 of ET-1 were attributed to activation of the ET(B) receptor.

11 a 1000-fold selectivity for the ET(A) vs the ET(B) receptor.

12 ONAs express mRNA for preproET-1, ET(A), and ET(B) receptors.

13 , these effects being mediated via ET(A) and ET(B) receptors.

14 nced cardiac clearance of ET-1, probably via ET(B) receptors.

15 d, consistent with a blockade of endothelial ET(B) receptors.

16 and ET(B)((-/-)) mice to confirm the loss of ET(B) receptors.

17 sized and evaluated for binding at ET(A) and ET(B) receptors.

18 rier and blocked, in addition, central ET(A)/ET(B) receptors.

19 radiation, is a ligand for the endothelin-B (ET(B)) receptor.

20 ally produce analgesia through endothelin-B (ET(B)) receptors.

21 ) = 40 pM) and highly selective for ET(A) vs ET(B) receptors (400 000-fold), with a half-life of >4 h

22 first evidence that stimulation of ET(A) and ET(B) receptors activate native PKC-dependent TRPC1 chan

23 The potential role of ET(B) receptor activation in these actions of ET-1-has n

24 a new endogenous analgesic circuit, in which ET(B) receptor activation induces the release of beta-en

25 These results establish that ET(B) receptor activation inhibits ET-1-induced pain beh

26 The present study demonstrates that ET(B) receptor activation may be a novel neuroprotective

27 1620 reversed these effects, indicating that ET(B) receptor activation reduces oxidative stress injur

28 ked by S6C, indicative of the involvement of ET(B) receptor activation.

29 xation, the signaling pathways downstream of ETB receptor activation are unknown.

30 e receptor 1 (CX3CR1), although whether ET-1/ETB receptor activation influences these events is unkno

31 Our aim was to define if ET-1/ETB receptor activation modulates CX3CL1/CX3CR1 signalin

32 r smooth muscle cells and vasorelaxation via ETB receptor activation of endothelial cells.

33 1), preproET-1, preproET-3, and both ETA and ETB receptors after rat carotid artery balloon angioplas

34 (ET-1, 1 pmol/L to 10 nmol/L), the selective ET(B) receptor agonist sarafotoxin (1 pmol/L to 10 nmol/

35 The ET(B) receptor agonist sarafotoxin 6c also reduced trans

36 ET(B) receptor agonist sarafotoxin also elicited concent

37 An ET(B) receptor agonist, sarafotoxin (S6c, 30 ng. kg(-1).

38 induced PMN adherence, whereas the selective ETB receptor agonist BQ-3020 mimicked the inhibitory act

39 te cells, ET-1 and sarafotoxin S6C (a potent ETB receptor agonist) stimulated stellate cell activatio

40 vasoconstriction to endothelin-1 (an ETA and ETB receptor agonist) was significantly blunted in CHF p

41 reas vasoconstriction to sarafotoxin S6c (an ETB receptor agonist) was significantly enhanced in CHF

42 agonist, 10 microg/min), or sarafotoxin S6c (ETB receptor agonist, 10 ng/min) was infused for 20 minu

43 xogenous Ala1,3,11,15 ET-1 (4 Ala ET-1), the ETB receptor agonist, and was blocked by the ETB recepto

44 Sarafotoxin S6C, an endothelin B (ETB) receptor agonist, had minor effects on portal press

45 eptor agonist, ET-3 and Sarafotoxin-S6c, two ETB receptor agonists, had little effect on cAMP accumul

46 th over 27 000-fold selectivity favoring the ET(B) receptor and an acceptable pharmacokinetic profile

47 r of ET(A) with significant affinity for the ET(B) receptor and shows excellent pharmacokinetic prope

48 ellular endothelin-1 activates endolysosomal ET(B) receptors and increase cytosolic Ca(2+) and nitric

49 The authors examined the roles of ET(A) and ET(B) receptors and of endothelin-converting enzyme (ECE

50 NOS) via pulmonary endothelial endothelin B (ET(B)) receptors and pulmonary intravascular macrophage

51 ted coupling of the Gq alpha subunits to the ETB receptor and did not support coupling of the Gi alph

52 This interaction and the role of ETB receptors and endothelial mediators were investigate

53 otein expression endpoints for dog ET(A) and ET(B) receptors, and, additionally, correlate ET recepto

54 s of identical experiments, combined ETA and ETB receptor antagonism provided only some of the protec

55 ade of ETA receptor, but it was inhibited by ETB receptor antagonism.

56 (3 and 10 nmol/min); and BQ-788, a selective ET(B) receptor antagonist (0.3 and 1 nmol/min) using ven

57 ist atrasentan (5 mg x kg(-1) x day(-1)), or ET(B) receptor antagonist A-192621 (15 mg x kg(-1) x day

58 An ET(B) receptor antagonist blocked effects of ET-1 and sa

59 Intravenous infusion of the ET(B) receptor antagonist BQ-788 caused a small but sign

60 ET(B) receptor antagonist BQ788 abolished vasoconstricti

61 ET(A) receptor antagonist BQ610, but not by ET(B) receptor antagonist BQ788, demonstrating that CNS-

62 eceptors for 28 days with only a mixed ET(A)/ET(B) receptor antagonist is insufficient to substantial

63 ficacy of SB 217242, a nonpeptide dual ET(A)/ET(B) receptor antagonist with high oral bioavailability

64 Bosentan, an oral endothelin ET(A)/ET(B) receptor antagonist, improves hemodynamics and exe

65 Intravenous pretreatment with another ET(A)/ET(B) receptor antagonist, L-754,142 (15 mg/kg as a bolu

66 ed by pretreatment with the endothelin ET(A)/ET(B) receptor antagonist, PD 145065 (48 micro g/2 micro

67 el by use of a potent, nonpeptide dual ET(A)/ET(B) receptor antagonist, SB 217242.

68 gest that bosentan, an oral endothelin ET(A)/ET(B) receptor antagonist, with or without concomitant p

69 1-fold control) and were inhibitable with an ET(B) receptor antagonist.

70 The drug BQ788 is an endothelin-B (ET(B)) receptor antagonist and inhibits upregulation of

71 gated by pretreatment with the endothelin B (ET(B)) receptor antagonist, BQ-788, but not by the endot

72 d proteins were blocked by an ET(A) (but not ET(B)) receptor antagonist.

73 ETB receptor agonist, and was blocked by the ETB receptor antagonist BQ 788 (n=3).

74 23 alone, and BQ-123 in combination with the ETB receptor antagonist BQ-788 after pretreatment with t

75 receptor antagonist, 10 microg/min), BQ-788 (ETB receptor antagonist, 10 microg/min), or sarafotoxin

76 Finally, the mixed endothelin-A (ETA) and ETB receptor antagonist, bosentan, reduced portal pressu

77 In contrast, preincubation with a selective ETB receptor antagonist, BQ788 (1 mumol/L) significantly

78 A selective ETB receptor antagonist, BQ788, was given for 2 weeks to

79 ffects of bosentan, an orally active ETA and ETB receptor antagonist.

80 which were not inhibited by either ET(A) or ET(B) receptor antagonists, respectively BQ-123 and BQ78

81 vel series of highly specific, orally active ET(B) receptor antagonists.

82 s been shown that highly potent combined ETA/ETB receptor antagonists can be developed from the C-ter

83 In conclusion, ET(A) and ET(B) receptors are differentially distributed in human

84 The hONAs expressed mRNA for ET(A) and ET(B) receptors as well as preproET-1, suggesting that t

85 vel mechanistic interaction between the ET-1/ETB receptor axis and CX3CL1/CX3CR1 in mediating pulmona

86 Selective ET(B) receptor blockade also decreased macrophage accumu

87 These effects were abolished by both ETB receptor blockade and NO synthase inhibition, wherea

88 Selective ETB receptor blockade, on the other hand, resulted in in

89 dothelin receptor blocker and by a selective ET(B) receptor blocker but was not inhibited by an ET(A)

90 issue is similar to that of the cloned human ETB receptor but different from that present in canine s

91 Blockade of ET(B) receptors by BQ788 followed by either vehicle or I

92 and after nonselective blockade of ET(A) and ET(B) receptors by combined infusion of BQ-123 (ET(A) bl

93 Both ETA and ETB receptors can mediate agonist-induced vasoconstricti

94 In contrast, blockade of ET(B) receptors caused inconsistent responses to exogeno

95 cells were stably transfected with ET(A) and ET(B) receptor cDNA.

96 The ETB receptor coupled effectively to both the Gi and Gq a

97 egeneration, Wistar-Kyoto wild type (WT) and ET(B) receptor-deficient (KO) rats were subjected to ret

98 ts of 60 mg/kg MCT in control (MCT(+/+)) and ET(B) receptor-deficient (MCT(sl/sl)) rats at 6 weeks of

99 idosis in vivo, the present studies examined ET(B) receptor-deficient mice, rescued from neonatal let

100 mined and thereafter showed that exposure of ET(B) receptor-deficient rats to the endothelial toxin m

101 laxin-treated nonpregnant rats was absent in ETB receptor-deficient rats, despite an increase in vasc

102 compared with controls and ET-1 triggered an ET(B) receptor dependent stimulation of eNOS in RPMVECs.

103 increases eNOS expression and activity in an ET(B) receptor-dependent manner in BPAECs.

104 nds with similar pharmacology, canine spleen ETB receptors displayed different molecular weight bands

105 Although canine lung and cloned human ETB receptors displayed the same molecular weight bands

106 ological effects via activation of ET(A) and ET(B) receptor (ET-R) subtypes.

107 Stimulation of both ET(A) and ET(B) receptors evoked channel activity which was inhibi

108 These data indicate that stimulation of ET(B) receptors evokes PKC-dependent TRPC1 activity thro

109 ed intraocular pressure mediated increase in ET(B) receptor expression and its activation may contrib

110 agonist, BQ-123, consistent with predominant ET(B) receptor expression.

111 In the current study, endothelin B (ET(B)) receptor expression was assessed in vivo, in the

112 T-1 and ETA expression are retained, whereas ETB receptor expression is reduced.

113 and expression of endothelin (ET) ET(A) and ET(B) receptors following cerebral ischemia produced in

114 ine the effect of selectively activating the ET(B) receptors following permanent middle cerebral arte

115 To determine the defect in more detail, ET(B) receptor fragments containing the N-terminal tail,

116 We examined this regulatory region of the ETB receptor gene (EDNRB) to determine whether hypermeth

117 m (BCE) for ET isoform and ET (i.e., ETA and ETB) receptor gene expression.

118 poptosis, while functional activation of the ETB receptor has protective effects.

119 Because ET(B) receptors have been shown to be targeted to endoly

120 ETA and ETB receptors have differential roles in CFVs: ETA recep

121 eport cryo-electron microscopy structures of ET(B) receptor in both its apo form and complex with RES

122 nd Western blotting showed expression of the ET(B) receptor in brain capillary membranes.

123 Collectively, these results implicate the ET(B) receptor in mediation of inflammatory pain and cut

124 ith A-192621 serve to reveal the role of the ET(B) receptor in modulating blood pressure; the observe

125 t an overall antiproliferative effect of the ET(B) receptor in pulmonary vascular homeostasis.

126 To examine the role of the ET(B) receptor in the response to acidosis in vivo, the

127 These demonstrate a critical role for the ET(B) receptor in the upregulation of MCAM by ET-1 and r

128 n ET(B) antagonist, to determine the role of ET(B) receptors in cerebral ischemia.

129 of acute nociceptive signaling by ET(A) and ET(B) receptors in cutaneous tissues.

130 We investigated functional significance of ET(B) receptors in mediating microhemodynamic effects of

131 To determine the role of ET(B) receptors in neurodegeneration, Wistar-Kyoto wild

132 We determined the distribution of ET(A) and ET(B) receptors in pulmonary arteries from pulmonary hyp

133 Norway rats produced increased expression of ET(B) receptors in the retina, mainly in retinal ganglio

134 ulated release of NO, a response mediated by ET(B) receptors in TM cells.

135 e of the signal peptide of the endothelin B (ET(B)) receptor in transiently transfected COS.M6 cells.

136 The role of endothelin B (ET(B)) receptors in inflammation and nociception was exa

137 provide evidence for the presence of a novel ETB receptor in different tissues as well as different s

138 We also compared the function of ETA and ETB receptors in healthy subjects and patients with CHF.

139 igands revealed similar small proportions of ETB receptors in the diseased and normal arterial media.

140 cts of IRL-1620, thus confirming the role of ETB receptors in the neurovascular remodeling actions of

141 These data suggest an important role for ETB receptors in the pathophysiology of pulmonary hypert

142 es that canine spleen possesses both ETA and ETB receptors in the ratio 65:35.

143 f endothelin-1 and endothelin A (ETA) and B (ETB) receptors in scleroderma-associated fibrotic lung d

144 In summary, binding of ET-1 to ET(B) receptors increases Na/H antiporter activity in OK

145 elial cells, activation of the endothelin-B (ET(B)) receptor increases NHE3 activity.

146 nd message expression profiles for ET(A) and ET(B) receptors indicated a disproportionate distributio

147 cts on the ET(A) receptor, because selective ET(B) receptor-induced stimulation with sarafotoxin rema

148 s were activated by endothelin-1 through the ETB receptor; inhibiting receptor-activated G-protein be

149 Selective ET(B) receptor inhibition in vivo significantly decrease

150 s 1 and 3, as well as a selective agonist of ETB receptor IRL-1620, equipotently stimulated migration

151 The endothelin B (ETB) receptor is a G-protein-coupled receptor, but the m

152 lammation and nociception was examined using ET(B) receptor knockout mice.

153 tion of endothelin A (ETA) and endothelin B (ETB) receptors leads to vasoconstriction and nitric oxid

154 ET-1 binding to sinusoidal endothelial cell ETB receptors led to increased protein kinase B/Akt phos

155 o significantly decreased pulmonary eNOS and ET(B) receptor levels and ameliorated HPS.

156 increase in pulmonary microvascular eNOS and ET(B) receptor levels and the onset of HPS.

157 No significant difference was observed in ET(B) receptor levels in any of the groups.

158 Deficiency of the ET(B) receptor markedly accelerates the progression of P

159 autocrine production of NO and suggest that ET(B) receptors may attenuate monocyte activity at sites

160 Recent studies indicate that ET(B) receptors may provide both vasodilatation and neur

161 onary artery segments had markedly increased ET(B) receptor mediated, nitric oxide dependent vasodila

162 In contrast, ET(B) receptor-mediated TRPC1 channel activity was inhib

163 otein-coupled receptor signaling pathway for ETB receptor-mediated NO production and call attention t

164 ism and ACE inhibition is synergistic via an ETB receptor-mediated, NO-dependent, COX-independent mec

165 time polymerase chain reaction for ET(A) and ET(B) receptor mRNA transcripts supported the site preva

166 Indeed, the presence of ET(B) receptor mRNA transcripts was detected in THP-1 an

167 The increase in ETB receptor mRNA occurred slightly earlier than the inc

168 A parallel but marked increase in ETA and ETB receptor mRNAs compared with preproET-1 and -3 messa

169 A green fluorescent protein-tagged ET(B) receptor mutant lacking the signal peptide was non

170 caused ET release and action through ETA and ETB receptors, nitric-oxide synthase, protein kinase C a

171 that endothelin-1 (ET-1), acting through an ET(B) receptor, NO synthase, and protein kinase C, rapid

172 eries with, and upstream of, the endothelial ETB receptor/NO signaling pathway in the renal vasodilat

173 by which relaxin stimulates the endothelial ETB receptor/NO vasodilatory pathway.

174 Thus, ET-1, acting through an ET(B) receptor, NOS, and PKC rapidly and reversibly redu

175 structural insight into RES-701-3 binding to ET(B) receptor offers valuable information for the devel

176 studied the effect of blocking or activating ET(B) receptors on ET-1-induced hindpaw flinching and ex

177 munohistochemistry revealed the emergence of ETB receptors on smooth muscle cells in the vasculature

178 ction, which coincides with the emergence of ETB receptors on smooth muscle cells.

179 n in skin, and establish keratinocytes as an ET(B) receptor-operated opioid pool.

180 endothelin-1 (ET-1) binding to endothelin B (ETB) receptors, overexpressed in the lung microvasculatu

181 These findings suggest that the ET-1/ET(B) receptor pathway contributes to melanoma developme

182 T) system demonstrate that deficiency of the ET(B) receptor predisposes adult rats to acute and chron

183 Immunohistochemistry revealed ET(A) and ET(B) receptors predominantly in smooth muscle and ECE-1

184 c sclerosis fibroblasts express both ETA and ETB receptors (predominantly ETA), but that ETA receptor

185 anine spleen poly(A)+ RNA indicated that the ETB receptor present in these tissues is functional and

186 n canine lung and the data indicate that the ETB receptor present in this tissue is similar to that o

187 In addition, the ETB receptors present in canine spleen were also identif

188 wnstream Dex-induced specific suppression of ET(B) receptor protein expression and declines in ET-1-m

189 However, Dex treatment diminished ET(B) receptor protein expression and produced a decreas

190 ern blot analysis showed that both ET(A) and ET(B) receptor proteins were present.

191 betes via activation of ET(A) receptors, and ET(B) receptors provide vasculoprotective effects.

192 ET-1 and ET-3 acted through the ETA and ETB receptors, respectively, and signaling through prote

193 In contrast, coinjection of an ET(B) receptor selective agonist, IRL-1620 (100 or 200 m

194 gesia in (+/+) mice was inhibited 74% by the ET(B) receptor-selective antagonist A192621 (25 mg/kg p.

195 An ET(B) receptor-selective antagonist, BQ-788 (3 mm), coin

196 e endothelin ETA receptor subtype because at ETB receptor-selective agonist, sarafotoxin S6c, was ine

197 a TNF-R1 receptor, released ET-1, activated ET(B) receptor signaling, and essentially abolished P-gl

198 through TNF-alpha release, ET-1 release, and ET(B) receptor signaling.

199 is of M. tuberculosis infections, and ETA or ETB receptor signaling can modulate the host response to

200 A novel ETB receptor splice variant (ETB-SVR) was identified fro

201 hat endothelin-1 binding to endothelial cell ETB receptors stimulates nitric oxide (NO) synthesis and

202 was abolished indicating that both ET(A) and ET(B) receptor stimulation activate this conductance.

203 increased intracellular cAMP levels, whereas ET(B) receptor stimulation selectively reduced cAMP leve

204 ing a positive feedback relationship between ETB receptor stimulation and ET protein expression.

205 diated leukocyte-endothelial interaction via ETB receptor stimulation and subsequent endothelial NO f

206 l roles in CFVs: ETA receptor antagonism and ETB receptor stimulation reduce CFVs, the latter at leas

207 showed enhanced selectivity, binding to the ETB receptor subtype in the micromolar range.

208 of small renal arteries via the endothelial ETB receptor subtype.

209 a potent antagonist, binding to the ETA and ETB receptor subtypes with affinities (IC50) of 0.4 and

210 m(2); p < 0.001) and a greater proportion of ET(B) receptors than proximal arteries (36 +/- 3% versus

211 hat have demonstrated functional coupling of ET(B) receptors to constitutive NO synthase activation.

212 treatment, suggesting functional coupling of ET(B) receptors to NO release.

213 demonstration of signaling from the occupied ETB receptor to constitutive nitric oxide (NO) synthase,

214 tic arteries, microautoradiography localized ETB receptors to neovascularization and, interestingly,

215 sion of a dopamine beta-hydroxylase promoter/ET(B) receptor transgene (Tg/Tg:ET(B)(-/-) mice).

216 state mRNA showed that whereas expression of ET(B) receptors was decreased in MCT(sl/sl) rat lungs, E

217 No change in expression of ET(B) receptors was observed following cerebral ischemia

218 both stretch sensitive and express ET(A) and ET(B) receptors, we tested the hypothesis that SIEH is d

219 The protein expression of ET(A) and ET(B) receptors were investigated by Western blot analys

220 receptor subtype characterization indicated ET(B) receptors were three times more prevalent in right

221 he specific binding sites for ET(A), but not ET(B), receptors were found in mixed pituitary cells and

222 ing in the VSMCs of the intimal layer, where ETB receptors were absent.

223 ETB receptors were detected on perivascular nerves and l

224 Gene expression of ET-1 and ETA but not ETB receptors were upregulated in the PVN and RVLM of E2

225 are deficient in intimal smooth muscle, and ETB receptors, where present, are found on endothelial c

226 and in culture express functional ET(A) and ET(B) receptors, which mediate ET-1-induced ERK (extrace

227 al responses via endothelin A (ET(A)) and B (ET(B)) receptors, which may form homo- and heterodimers

228 hinese hamster ovary cells stably expressing ETB receptor with or without endothelial NO synthase, an

229 indicated a disproportionate distribution of ET(B) receptors within right coronary artery of dog and