ライフサイエンスコーパス: bradykinin

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

2 tic neurons electrically hyper-responsive to bradykinin.

3 f bioactive peptides such as neurotensin and bradykinin.

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

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

6 indlimb vasodilatation to the ACE substrate, bradykinin.

7 which they are chemotactically attracted by bradykinin.

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

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

10 activated pKal and FXII cleave HK to release bradykinin.

11 injury and lack the proinflammatory mediator bradykinin.

12 of a failure to control local production of bradykinin.

13 were stimulated either mechanically or with bradykinin.

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

15 e high molecular weight kininogen to produce bradykinin.

16 lium-dependent vasorelaxation in response to bradykinin.

17 ates the kallikrein-kinin system, increasing bradykinin.

18 10.1 +/- 0.8% for the octapeptide des-Arg(1)-bradykinin.

19 impulse firing and channel sensitization by bradykinin.

20 welling attacks caused by elevated levels of bradykinin.

21 yzes kininogen, leading to the liberation of bradykinin.

22 ndothelial cells in response to NO donors or bradykinin.

23 ikrein-HK complex to generate kallikrein and bradykinin.

24 ininogen (HK) and release of proinflammatory bradykinin.

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

26 asodilator and the pro-inflammatory peptide, bradykinin.

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

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

29 3-fold to angiotensin II (10(-8) mol/L), and bradykinin (10(-4) mol/L) induced reduction of myocardia

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

31 ry neurons during concomitant application of bradykinin, a key inflammatory mediator formed during ti

32 plasma, which can lead to the generation of bradykinin, a potent vasoactive mediator.

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

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

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

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

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

38 yogenic tone and dilated dose dependently to bradykinin, adenosine, and sodium nitroprusside.

39 o endothelium-dependent NO-mediated agonists bradykinin and A23187 but not to endothelium-independent

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

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

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

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

44 en can be hydrolysed by plasma kallikrein to bradykinin and cleaved high-molecular-weight kininogen (

45 hibitor L-NAME nearly abolished dilations to bradykinin and flow and attenuated the adenosine-induced

46 ma and the direct propermeability actions of bradykinin and histamine were reduced dramatically in Ak

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

48 stance P exhibited similar responsiveness to bradykinin and histamine.

49 Isolated human retinal arterioles dilate to bradykinin and increased flow in an NO-dependent manner.

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

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

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

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

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

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

56 amino-terminal X-Pro bond of the nonapeptide bradykinin and of two globin pentapeptides that are pote

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

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

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

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

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

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

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

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

65 induced by GPCR agonists (e.g., neurotensin, bradykinin, and angiotensin II).

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 t group of vasoactive peptides (angiotensin, bradykinin, and related hormones) in 50-microl plasma sa

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

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

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

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

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

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

77 cked NGF treatment and sensitized neurons to bradykinin application.

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

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

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

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

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

83 rons, muscarinic M(1), angiotensin II AT(1), bradykinin B(2) and purinergic P2Y agonists suppress M c

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

85 crossover study comparing the effect of the bradykinin B(2) receptor blocker HOE-140 with vehicle on

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

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

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

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

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

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

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

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

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

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

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

97 30 mg of subcutaneous icatibant, a selective bradykinin B2 receptor antagonist, or to the current off

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

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

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

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

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

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

104 ever, chronic ACE inhibition caused a marked bradykinin/B2 receptor-mediated increase in LV ISF chyma

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

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

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

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

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

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

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

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

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

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

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

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

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

118 Chemoattractant bradykinin (BK) stimulated microglial migration by incre

119 shown previously that the vasoactive peptide bradykinin (BK) stimulates proliferation of a cultured m

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

121 Bradykinin (BK), at concentrations corresponding to the

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

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

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

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

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

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

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

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

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

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

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

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

134 Pretreatment with intraplantar galanin and bradykinin, compounds known to sensitize TRPV1 receptors

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

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

137 ether, these results suggest that endogenous bradykinin contributes to increases in MCP-1 and PAI-1 a

138 To test the hypothesis that bradykinin contributes to the inflammatory and fibrinoly

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 Our results demonstrate bradykinin-dependent activation and repression, respecti

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

146 on, whereas expression of DN-XBP-1 inhibited bradykinin-dependent IL-8 secretion.

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

148 imental and beneficial effects of endogenous bradykinin during hemodialysis has implications for the

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

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

151 Finally, A23187- or bradykinin-enhanced AMPK activation was significantly gr

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

153 However, bradykinin failed to alter cold sensitivity even though

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

155 h K(m) values, this suggests low affinity of bradykinin for IDE.

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

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

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

159 Although bradykinin formation is typically initiated by factor XI

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

161 C1 esterase inhibitor, and elicit excessive bradykinin formation.

162 intensity of contact system activation, and bradykinin formation.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

183 neate neurons responding to intrapericardial bradykinin (IB, 15.6%, 17/109) was significantly less th

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

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

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

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

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

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

190 ed ER/Ca(2+) store expansion and potentiated bradykinin-increased interleukin (IL)-8 secretion, where

191 These results suggest a novel mechanism of bradykinin-independent kallikrein action that may contri

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

212 Bradykinin is not only important for inflammation and bl

213 Bradykinin is the most potent endogenous inducer of acut

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

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

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

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

218 Bradykinin may play a role in the autodigestive disease

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

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

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

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

227 osphorylated vimentin, while the cleavage of bradykinin-mimetic peptide by IDE is increased 2- to 3-f

228 eta degradation but monophasic for a shorter bradykinin-mimetic substrate.

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

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

231 Factors that increase the production of bradykinin or decrease its degradation may enhance the i

232 eptidase to generate B1R agonists des-Arg(9)-bradykinin or des-Arg(10)-kallidin.

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

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

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

240 Quantitative labeling of bradykinin peptide was accomplished with a commercially

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

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

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

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

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

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

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

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

249 Bradykinin promotes inflammation but also stimulates end

250 pain perception in AQP1(-/-) mice evoked by bradykinin, prostaglandin E(2), and capsaicin as well as

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

252 ASIC1a activity is independent of opioid or bradykinin receptor activation but is prevented in the p

253 Bradykinin receptor antagonism did not affect the mean a

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 Absence of the bradykinin receptors also enhances the diabetes-associat

261 he authors report that the stimulation of B2 bradykinin receptors by bradykinin triggers the release

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

263 , which acts via G protein-coupled B1 and B2 bradykinin receptors on VSMCs and endothelial cells.

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

265 res kallikrein activity but does not involve bradykinin receptors.

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

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

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

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

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

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

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

273 Bradykinin stimulated transendothelial migration of EPCs

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

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

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

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

278 an apparent 10-fold increase in vasodilatory bradykinin that reversed after drug infusion but relativ

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

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

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

282 mation of angiotensin II, and degradation of bradykinin, thus regulating blood pressure and renal han

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

284 he stimulation of B2 bradykinin receptors by bradykinin triggers the release of intracellular calcium

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

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

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

288 ty was also inhibited in the presence of the bradykinin type 2 receptor antagonist HOE140, without af

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

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

291 to baseline of [Ca](i) after stimulation by bradykinin was delayed by approximately 50% in ASM cells

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

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

294 lium-dependent vasorelaxation in response to bradykinin was reduced significantly by the ritonavir in

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 allikrein (KK) are thought to be mediated by bradykinin, which acts via G protein-coupled B1 and B2 b

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