ライフサイエンスコーパス: bradykinin

1 lecular weight kininogen and elevated plasma bradykinin.

2 welling attacks caused by elevated levels of bradykinin.

3 yzes kininogen, leading to the liberation of bradykinin.

4 ndothelial cells in response to NO donors or bradykinin.

5 ininogen (HK) and release of proinflammatory bradykinin.

6 rons and counteracts PIEZO2 sensitization by bradykinin.

7 bitor (C1-INH), leading to overproduction of bradykinin.

8 asodilator and the pro-inflammatory peptide, bradykinin.

9 but had no effect on the response induced by bradykinin.

10 tic neurons electrically hyper-responsive to bradykinin.

11 f bioactive peptides such as neurotensin and bradykinin.

12 ed to histamine, and about half responded to bradykinin.

13 pecies-specific ID LC-ICPMS determination of bradykinin.

14 indlimb vasodilatation to the ACE substrate, bradykinin.

15 which they are chemotactically attracted by bradykinin.

16 el peptides substance P, angiotensin II, and bradykinin.

17 en and reduces airway hyperresponsiveness to bradykinin.

18 kininogen (HK) and can digest HK to produce bradykinin.

19 , the precursor to the permeability mediator bradykinin.

20 rives production of the inflammatory peptide bradykinin.

21 injury and lack the proinflammatory mediator bradykinin.

22 of a failure to control local production of bradykinin.

23 were stimulated either mechanically or with bradykinin.

24 inal Arg) but generated a response to Lys(9)-bradykinin.

25 h molecular weight kininogen (HK) to release bradykinin.

26 nogen (HK), releasing the vasoactive peptide bradykinin.

27 ikrein-HK complex to generate kallikrein and bradykinin.

28 activated pKal and FXII cleave HK to release bradykinin.

29 impulse firing and channel sensitization by bradykinin.

30 elatively much higher than BCM 5 (0.03%) and bradykinin (0.1%).

31 al vascular problem because of activation of bradykinin 1 receptor (B1R) and B2R on endothelial cells

32 e left ventricle to administer a solution of bradykinin (10 microg/ml, 0.2 ml, 1 min).

33 endothelium-dependent vasorelaxation to BK (bradykinin; 10(-)(6)-10(-)(10) M) was blunted (P<0.05) i

34 rioles from aged rats (maximal relaxation to bradykinin: 56.4 +/- 5.1% vs. 75.3 +/- 5.2%, OSED vs. YS

35 Lack of C1-INH leads to overproduction of bradykinin, a potent vasoactive peptide.

36 Bradykinin, a proalgesic agent released during inflammat

37 ded NGF and compared their responsiveness to bradykinin, a proinflammatory peptide.

38 fusions when astrocytes were stimulated with bradykinin, a stimulus otherwise resulting in more full

39 Mediators such as histamine and bradykinin act directly on venules to increase the perme

40 the kallikrein-kinin system are mediated by bradykinin acting on B1 and B2 bradykinin receptors.

41 bradykinin receptors (to prevent downstream bradykinin action).

42 substrates, such as caspase-1 substrate and Bradykinin-analog.

43 Several peptide hormones including bradykinin and angiotensin I have been described as subs

44 for several molecular species-two peptides, bradykinin and angiotensin II; two lipids, phosphatidylc

45 3) upon induction by different inducers like Bradykinin and ATP.

46 ed B1R-dependent NO production stimulated by bradykinin and blocked the increased endothelial permeab

47 act system produces the inflammatory peptide bradykinin and contributes to experimental thrombosis.

48 n (PKa), which cleaves kininogens to release bradykinin and converts the protease precursor factor XI

49 ory mediators including acetylcholine (ACh), bradykinin and histamine-also termed airway hyper-respon

50 stance P exhibited similar responsiveness to bradykinin and histamine.

51 he contact system, triggering high levels of bradykinin and increased vascular permeability, but the

52 Here we newly investigate the role of bradykinin and its B2 receptor for the recruitment and f

53 RECENT FINDINGS: Decreased degradation of bradykinin and its metabolites is thought to be a culpri

54 tion assay was used to determine the role of bradykinin and its receptor in EPC mobilization.

55 The importance of bradykinin and its receptors in mediating these response

56 ependent nitric oxide (NO)-mediated agonists bradykinin and L-lactate were significantly reduced only

57 f other substrates including the vasodilator bradykinin and N-acetyl-Ser-Asp-Lys-Pro (Ac-SDKP), a phy

58 ts via depletion of PIP(2), whereas the B(2) bradykinin and P2Y purinergic types elicit robust IP(3)-

59 helial permeability caused by treatment with bradykinin and pyrogallol (a superoxide generator).

60 nd u46619 levels and relaxation responses to bradykinin and sodium nitroprusside were assessed at day

61 elium-dependent NO-mediated vasodilations to bradykinin and stepwise increases in luminal flow were s

62 dependent on plasmin-mediated generation of bradykinin and subsequent activation of bradykinin B2 re

63 Here we describe novel functions for bradykinin and the kinin-B2 receptor (B2BkR) in differen

64 presence of IMs (in mum: 1 prostaglandin, 10 bradykinin, and 1 histamine) using whole-cell and perfor

65 tasis, cleaves the vasoactive angiotensin-I, bradykinin, and a number of other physiologically releva

66 of autologous blood, plasma kallikrein (PK), bradykinin, and collagenase were performed in Sprague-Da

67 ted by several compounds including thrombin, bradykinin, and histamine.

68 eave proinflammatory mediators, such as C5a, bradykinin, and osteopontin.

69 on lysophosphatidic acid, purinergic (ATP), bradykinin, and protease-activated (thrombin) receptors.

70 s of these antagonists on resting FBF and on bradykinin- and acetylcholine-mediated vasodilation were

71 vicious positive feedback loop of des-Arg(9)-bradykinin- and bradykinin-mediated inflammation -> inju

72 s sections were determined for tetraglycine, bradykinin, angiotensin 2, melittin, and ubiquitin at 30

73 scriptomes and show that key elements of the bradykinin, angiotensin and coagulation systems are co-e

74 trosprayed C2-C12 tetra-alkyl ammonium ions, bradykinin, angiotensin I, angiotensin II, bovine ubiqui

75 own substrates such as plasma prekallikrein, bradykinin, angiotensins II and III, and alpha-MSH, sugg

76 ril, are unclear, although a contribution of bradykinin appears likely.

77 tion potentials, and Ca(2+) elevations after bradykinin application, whereas neurons cultured without

78 cked NGF treatment and sensitized neurons to bradykinin application.

79 uch as dodecyl trimethylammonium bromide and bradykinin are estimated to be approximately 16 and appr

80 ed migration in response to the neuropeptide bradykinin are largely unknown.

81 basal transport mechanism was studied using bradykinin as control as it shows resistance to cellular

82 alanced control of kallikrein activity, with bradykinin as most likely mediator.

83 ne, Pro-Leu-Gly tripeptide, and [Des-Arg(9)]-bradykinin as the model compounds.

84 endothelial-dependent relaxation response to bradykinin at day 10 postinfection.

85 safety of single injections of icatibant, a bradykinin B(2) receptor antagonist, in the treatment of

86 Icatibant, a bradykinin B(2) receptor antagonist, promotes MC degranu

87 Recent studies demonstrated a role for the bradykinin B1 receptor (B1R) in cognitive deficits induc

88 Bradykinin B1 receptor (B1R) is a G-protein-coupled rece

89 )-coupled prostaglandin-EP2 and G(q)-coupled bradykinin B2 (BK2) receptors.

90 M-channel opener retigabine, or agonists of bradykinin B2 or purinergic P2Y receptors on the SNs.

91 differential dynamic regulation of endosomal bradykinin B2 receptor (B2R) complexes with either beta-

92 targeting of the C5a receptor (C5aR) or the bradykinin B2 receptor (B2R) inhibited plasma leakage in

93 inhibitors are partly mediated by increased bradykinin B2 receptor activation, this study aimed to d

94 in December 2009) and icatibant (a selective bradykinin B2 receptor antagonist approved for use in th

95 hibitor l-N(6)-nitroarginine methyl ester or bradykinin B2 receptor antagonist icatibant.

96 tudy does not support clinical efficacy of a bradykinin B2 receptor antagonist in ACE inhibitor-assoc

97 We sought to test the hypothesis that a bradykinin B2 receptor antagonist would shorten time-to-

98 Icatibant, a bradykinin B2 receptor antagonist, is an established tre

99 30 mg of subcutaneous icatibant, a selective bradykinin B2 receptor antagonist, or to the current off

100 ein, high-molecular-weight kininogen, or the bradykinin B2 receptor, but not the B1 receptor, largely

101 Bradykinin B2 receptor-deleted mice (Bdkrb2(-/-)) have d

102 n of bradykinin and subsequent activation of bradykinin B2 receptors.

103 (I(M)) suppression by muscarinic M1, but not bradykinin B2, receptors.

104 lex formation between angiotensin II AT1 and bradykinin B2, two G protein-coupled receptors with oppo

105 ion mediated by another Gq-coupled receptor, bradykinin B2.

106 Treatment with icatibant (bradykinin-B2-antagonist) or anakinra (interleukin-1-ant

107 Bradykinin-B2-receptor (B2R) blockade by icatibant subst

108 We newly report that bradykinin/B2R signaling may promote endothelial repair

109 AS) to histamine (HA), serotonin (5-HT), and bradykinin (BDK).

110 aling of the alpha(2) adrenergic receptor or bradykinin BK(2) receptor, suggesting the development of

111 ng microvascular endothelial cells (HLMVEC), bradykinin (BK) activates kinin B2 receptor (B2R) signal

112 s high-molecular-weight kininogen to release bradykinin (BK) and is a key constituent of the proinfla

113 ity between Dyn A and endogenous BR ligands, bradykinin (BK) and kallidin (KD), this interaction coul

114 The bradykinin (BK) B1 receptor is an attractive target for

115 DRG cultures with the inflammatory mediator bradykinin (BK) caused robust trafficking of heterologou

116 ment enhanced acute contractile responses to bradykinin (BK) in isolated rat bronchioles, and inhibit

117 CSAR activation by epicardial application of bradykinin (BK) increased heart rate (HR), left ventricu

118 Bradykinin (Bk) is a potent inflammatory mediator that c

119 Bradykinin (BK) is one of the most potent vasodilator ag

120 connexin-32 (Cx32) and Cx43 were exposed to bradykinin (BK) or ATP to induce Ca(2+) oscillations.

121 Chemoattractant bradykinin (BK) stimulated microglial migration by incre

122 asma and loss of TM-stimulated conversion of bradykinin (BK) to des-Arg(9)-BK by TAFIa in normal plas

123 iators, such as prostaglandin E(2) (PGE(2)), bradykinin (BK), and nerve growth factor (NGF) as well a

124 Bradykinin (BK), at concentrations corresponding to the

125 tack is believed to lead to the formation of bradykinin (BK), which increases local vasopermeability

126 ular weight kininogen (HK) is a precursor of bradykinin (BK).

127 pectrometry (IM-MS) study of the nonapeptide bradykinin (BK, amino acid sequence Arg(1)-Pro(2)-Pro(3)

128 onal space of the N-terminal 1-5 fragment of bradykinin (BK[1-5](2+)) in the gas phase by combining d

129 Third, bradykinin, but not acetylcholine, stimulates K(+)(Ca) c

130 I(M) suppression by purinergic agonist or by bradykinin, but reduced I(M) suppression by muscarinic a

131 ons of B2R protein expression induced by NO, bradykinin, C1-INH, or icatibant unlikely contribute to

132 Prostaglandin E2 and bradykinin can activate airway sensory nerves via EP3 an

133 strated with a mixture of angiotensin II and bradykinin cations.

134 matory mediators such as prostaglandin-E2 or bradykinin cause hyperalgesia by activating cellular kin

135 ation of TLC-S and the inflammatory mediator bradykinin caused more extensive necrosis in both stella

136 en Mycoplasma pulmonis, or iv) leakage after bradykinin challenge in the presence of vascular stabili

137 Pathophysiologically relevant bradykinin concentrations consistently evoked Ca(2+) sig

138 from three procedure blanks was obtained for bradykinin, confirming the suitability of the method for

139 iac signal transduction involves: adenosine, bradykinin, cytokines, and chemokines, which activate sp

140 in the pathways of bradykinin formation and bradykinin degradation in the plasma of patients with HA

141 Bradykinin degradation was markedly abnormal in 1 of 23

142 Bradykinin degradation was normal in all but 1 of 23 pat

143 This pathway arises when bradykinin delivery to vasculature is compromised and me

144 mononuclear cells substantially impairs the bradykinin-dependent endothelial repair, representing a

145 These bradykinin-driven outcomes explain many of the symptoms

146 ide strategies for developing treatments for bradykinin-driven pathologies.

147 Our findings suggest a pivotal role of bradykinin during glioma invasion by stimulating amoeboi

148 In this study, we have investigated bradykinin-elicited Ca(2+) signal generation in normal m

149 The bradykinin-elicited Ca(2+) signals were due to initial C

150 Application of bradykinin every 10-min on the gallbladder induced consi

151 However, bradykinin failed to alter cold sensitivity even though

152 trate Mca-RPPGFSAFK(Dnp)-OH, a derivative of bradykinin, following preincubation with metal chelate-l

153 evidence of abnormalities in the pathways of bradykinin formation and bradykinin degradation in the p

154 s with hereditary angioedema, kallikrein and bradykinin formation can occur without invoking factor X

155 Our findings indicate a new pathway for bradykinin formation in patients with HAE, in which FXII

156 Although bradykinin formation is typically initiated by factor XI

157 P derived from RBL-2H3 mast cells stimulated bradykinin formation, and it was also detected in human

158 intensity of contact system activation, and bradykinin formation.

159 C1 esterase inhibitor, and elicit excessive bradykinin formation.

160 ascertained by inhibition of enzymes of the bradykinin-forming cascade, namely factor XIIa and kalli

161 II, resulting in excessive activation of the bradykinin-forming kallikrein-kinin pathway.

162 We investigated bradykinin-forming pathways in blood plasma with newly d

163 The sensitivity of HA-LAESI for the polar bradykinin fragment 1-8 was slightly lower than observed

164 rylin, 1,1',2,2'-tetramyristoyl cardiolipin, bradykinin fragment 1-8, and 1-palmitoyl-2-oleoyl-sn-gly

165 vascular permeability due to the release of bradykinin from high molecular weight kininogen.

166 In addition to releasing bradykinin from HK, Kal directly activated monocytes to

167 an glioma cells whose migration is guided by bradykinin generate bleb-like protrusions.

168 is and support the hypothesis that targeting bradykinin generation and signaling provides a novel and

169 elude for initiating the cascades that drive bradykinin generation and the intrinsic pathway of coagu

170 Here we show a strategy to block bradykinin generation by using an HK antibody that binds

171 An FXII-neutralizing antibody abolished bradykinin generation in HAEIII patient plasma and blunt

172 ion, Desmolaris binds kallikrein and reduces bradykinin generation in plasma activated with kaolin.

173 inhibitor and consequently exhibit excessive bradykinin generation that in turn causes debilitating a

174 A link between excessive fibrinolysis and bradykinin generation that is estrogen dependent is sugg

175 In agreement with these preclinical data, bradykinin generation was also observed in humans in a c

176 es is demonstrated using model peptide ions (bradykinin, gramicidin S, and trpzip 1).

177 cytes expressing SNAP25B and stimulated with bradykinin had a reduction in decay slope.

178 s that prevent the generation or activity of bradykinin have been developed for the treatment of HAE

179 The endothelial-supportive effects of bradykinin have mainly been attributed to activation of

180 n of endothelial cells (ECs), the targets of bradykinin, have not yet been studied during HAE attacks

181 tracheal blood vessels at baseline or after bradykinin; however, AX102 exaggerated leakage at 7 days

182 one) and large peptides having m/z >/= 1000 (bradykinin, ICNKQDCPILE) without the interference from m

183 baseline, ii) acute inflammation induced by bradykinin, iii) sustained inflammation after 7-day infe

184 d in cells subjected to L-NA, NO donors, and bradykinin in a time- and concentration-dependent manner

185 Treatment of gliomas with bradykinin in situ increased glioma growth by increasing

186 ue kallikrein-1, the protease that generates bradykinin in situ, is much less understood.

187 Neurogenesis was augmented by bradykinin in the middle and late stages of the differen

188 ections of either PK or collagenase, but not bradykinin, induce retinal hemorrhage in rats.

189 In aortic rings of C57BL/6 mice, bradykinin induced B2R-dependent constrictions which wer

190 C1-INH, or icatibant unlikely contribute to bradykinin-induced angioedema.

191 no effect on B2 receptor ligand affinity or bradykinin-induced arrestin3 recruitment.

192 ntly, inhibition of either channel abrogates bradykinin-induced chemotaxis and reduces tumor expansio

193 ARHGEF1, an activator of RhoA, as well as on bradykinin-induced contraction, in airway smooth muscle.

194 evation of vascular superoxide and preserved bradykinin-induced dilation.

195 on porcine coronary arteries, RA-2 inhibited bradykinin-induced endothelium-derived hyperpolarization

196 s mitochondrial Ca(2+) uptake in response to bradykinin-induced ER Ca(2+) release, indicating that PC

197 s finding does not rule out a role for NO in bradykinin-induced extravasation and/or angioedema.

198 NGF did not alter bradykinin-induced M-current inhibition or phosphatidyli

199 in glial protein expression, indicating that bradykinin-induced receptor activity contributes to neur

200 on and contraction, but partially suppressed bradykinin-induced RhoA activity (RhoA-GTP content).

201 TGF-beta enhanced bradykinin-induced RhoA translocation, Rho-kinase-depend

202 iability and proliferation, we conclude that bradykinin-induced signaling provides a switch for neura

203 ancreatic damage can be further escalated by bradykinin-induced signals in stellate cells and thus ki

204 Liu et al. suggest a new mechanism via which bradykinin induces acute spontaneous pain.

205 Animals exposed to intraplantar formalin or bradykinin injection exhibited CASP6 activation in the d

206 imulating peptide angiotensin II and cleaves bradykinin into inactive peptides.

207 Bradykinin is a potent part of the vasopressor system th

208 Bradykinin is a proinflammatory factor that mediates ang

209 dictable attacks of tissue swelling in which bradykinin is implicated.

210 Bradykinin is not only important for inflammation and bl

211 Bradykinin is the most potent endogenous inducer of acut

212 hat in sensory neurons PLCbeta activation by bradykinin led to a moderate decrease in phosphatidylino

213 ation of biomolecules in droplets containing bradykinin, leucine enkephalin and myoglobin, but loss o

214 natural product ebelactone B increased renal bradykinin levels and prevented the development of salt-

215 l pattern of the RAS is predicted to elevate bradykinin levels in multiple tissues and systems that w

216 ekallikrein to plasma kallikrein, leading to bradykinin liberation, and degrades angiotensin II.

217 Bradykinin may play a role in the autodigestive disease

218 ulitis in patients with recurrent wheals and bradykinin-mediated angioedema in patients with recurren

219 te-use pilot study, two patients with severe bradykinin-mediated angioedema were initially administer

220 Bradykinin-mediated angioedema, which includes hereditar

221 utcomes for patients with different forms of bradykinin-mediated angioedema.

222 d are also being evaluated in other types of bradykinin-mediated angioedema.

223 on levels of neural markers, suggesting that bradykinin-mediated effects are exclusively mediated via

224 feedback loop of des-Arg(9)-bradykinin- and bradykinin-mediated inflammation -> injury -> inflammati

225 IL-6 had no effect on bradykinin-mediated IP accumulation, suggesting that reg

226 with mast cell mediator-induced (n = 49) or bradykinin-mediated recurrent AE (n = 48).

227 Both L-NMMA and TEA attenuated bradykinin-mediated vasodilation in healthy and hypercho

228 bitor intake and hereditary angioedema (both bradykinin-mediated).

229 Drug development for bradykinin-meditated pathologies has focused on designin

230 angiotensin-converting enzyme is inhibited, bradykinin metabolism is dependent on degradation by neu

231 rting enzyme (ACE) can cleave angiotensin I, bradykinin, neurotensin and many other peptide substrate

232 Na(+)/K(+)ATPase, inducing natriuresis in a bradykinin-nitric oxide-cGMP-dependent manner.

233 tor signaling via CPM-mediated conversion of bradykinin or kallidin to des-Arg kinin B1R agonists.

234 icient B1R signaling by B2 receptor agonists bradykinin or kallidin.

235 Angioedema may be mediated by histamine, bradykinin or other mediators.

236 mellipodia and filopodia formation following bradykinin or PDGF stimulation.

237 Application of MGO together with bradykinin or prostaglandin E(2) resulted in an overaddi

238 Conversely, co-application of bradykinin or the P2Y-receptor agonist UTP augmented the

239 increase in [Ca(2+)](i) using thapsigargin, bradykinin, or acetylcholine can increase hemidesmosomes

240 ht kininogen, generating the proinflammatory bradykinin peptide and additional high molecular weight

241 Quantitative labeling of bradykinin peptide was accomplished with a commercially

242 MS SI restoration for the Z-Gly-Gly-Val and bradykinin peptides were 75-83% while % MS SI reduction

243 ely hyperglycemic rats, whereas injection of bradykinin, plasmin or tissue plasminogen activator did

244 moting agents and we therefore conclude that bradykinin plays a role in acute pancreatitis via specif

245 ty of the natural peptide inhibitors of ACE, bradykinin potentiating peptide b and Ang II.

246 rypsin-modulating oostatic factor/TMOF and a bradykinin-potentiating peptide, BPP-12b) were all inhib

247 r FXII activation, which causes uncontrolled bradykinin production in patients with FXII-HAE.

248 nd -SLLR/V are superior to C1INH in reducing bradykinin production in plasma.

249 leaves HK and induces a dramatic increase in bradykinin production, our HK antibody blocked these eve

250 ing that factor XII (FXII) levels may affect bradykinin production, we investigated the contribution

251 xtran sodium sulfate-induced HK cleavage and bradykinin production.

252 To test if bleb formation is related to bradykinin-promoted glioma invasion we blocked glioma mi

253 patch-clamp electrophysiology, we find that bradykinin raises [Ca(2+)](i) and induces a biphasic vol

254 Recently, icatibant, a bradykinin receptor antagonist, has been used to success

255 The bradykinin receptor B1R is overexpressed in many human c

256 n mediated the enhancing action of purine or bradykinin receptor stimulation on eNOS Ser-635/633 phos

257 at have been reported to reside in caveolae, bradykinin receptor type 2 (B(2)R), which is coupled to

258 efore explored the influence of lack of both bradykinin receptors (B1R and B2R) on diabetic nephropat

259 regulated dynorphin A (Dyn A) interacts with bradykinin receptors (BRs) in the spinal cord to promote

260 kinin release) or antagonists of endothelial bradykinin receptors (to prevent downstream bradykinin a

261 Absence of the bradykinin receptors also enhances the diabetes-associat

262 (STIA) model, mice that lacked HK, pKal, or bradykinin receptors displayed protective phenotypes in

263 on day 1 postinjury, whereas the increase in bradykinin receptors was gradual after day 3 postinjury.

264 e mediated by bradykinin acting on B1 and B2 bradykinin receptors.

265 allikrein enzymes that activate it, and both bradykinin receptors.

266 res kallikrein activity but does not involve bradykinin receptors.

267 Ang1-9 stimulates bradykinin release in endothelium and has antihypertroph

268 d plasma kallikrein generation and excessive bradykinin release resulting from cleavage of high-molec

269 rs to the enzymes that cleave HK (to prevent bradykinin release) or antagonists of endothelial bradyk

270 o HK, preventing its cleavage and subsequent bradykinin release.

271 cific manner, resulting in the appearance of bradykinin-responsive neuronal subclasses that are relev

272 viously unreported increase in the number of bradykinin-responsive neurons, with larger increases obs

273 tion of KNG-deficient mice with human KNG or bradykinin restored clot deposition and infarct suscepti

274 CPM-E264Q-mediated activation of B1Rs by bradykinin resulted in increased intramolecular fluoresc

275 Moreover, bradykinin selectively up-regulated expression of the ho

276 ng intra-arterial infusion of acetylcholine, bradykinin, sodium nitroprusside, and verapamil.

277 -time-of-flight (TOF)-MS against an internal bradykinin standard.

278 Bradykinin stimulated transendothelial migration of EPCs

279 -stimulated Ca(2+) oscillations and BAECs to bradykinin-stimulated Ca(2+) oscillations.

280 of B2R with silencing RNA completely blocked bradykinin-stimulated transendothelial migration.

281 av1 ablates the prolonged recovery seen upon bradykinin stimulation in accord with the idea that the

282 a and filopodia formation following PDGF and Bradykinin stimulation, respectively.

283 creased by metoprolol/ramipril or metoprolol/bradykinin (the latter increased after ACE inhibitor int

284 Although angioedema is induced by bradykinin, the function and activation of endothelial c

285 ole in RAAS is needed to inactivate des-Arg9 bradykinin, the potent ligand of the B1R.

286 was shown to cleave high m.w. kininogen into bradykinin; therefore, we hypothesized that MASP-1 level

287 sed on the determination of phenylalanine in bradykinin to derive the concentration of the peptide in

288 d vacuoles and expressed increased levels of bradykinin type 2 receptor (B2R) and progenitor cell mar

289 -mediated angioedema including variations in bradykinin type 2 receptor (B2R) expression and activity

290 ulation of Galphaq and one of its receptors, bradykinin type 2 receptor (B2R), as well as a significa

291 erefore likely mediated by overactivation of bradykinin type 2 receptors (B2).

292 Bradykinin was added to plasma, and its rate of degradat

293 were hydrolyzed by cellular peptidases while bradykinin was found intact.

294 Aortic reactivity to bradykinin was investigated including eNOS(-/-) mice.

295 phosphoethanolamine (DPPE), cholesterol, and bradykinin were greatly increased using IL matrices.

296 f intracellular calcium (iCa) in response to bradykinin were monitored in porcine and murine endothel

297 OPT2 while BCM 5, its hydrolytic product and bradykinin were suggested to be transported mainly via t

298 nuclear factor kappaB (NF-kappaB) induced by bradykinin, whereas mutation of the NLS reduced this eff

299 h-molecular-weight kininogen (HK) to release bradykinin with a catalytic efficiency ~1500-fold lower

300 C-terminal Lys inhibited the B1R response to bradykinin (with C-terminal Arg) but generated a respons