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1 ity to bacterial toxins, and blockade by the B2 receptor antagonist.
2 evented by icatibant, a clinically available B2 receptor antagonist.
3 cell proliferation was also inhibited by the B2 receptor antagonist alone (27%) but not by the NK1 re
5 2009) and icatibant (a selective bradykinin B2 receptor antagonist approved for use in the United St
6 17647 and Hoe 140 (p < 0.05), two bradykinin B2 receptor antagonists, but not by desArg9,[Leu8]bradyk
7 as significantly inhibited by the bradykinin B2 receptor antagonist, d-Arg, [Hyp3, Thi5,8, d-Phe7]-br
13 to bradykinin was blocked by the bradykinin B2 receptor antagonist HOE 140, by inhibition of the Ca2
14 rd current response to Bk was blocked by the B2 receptor antagonist HOE-140, which indicates that the
17 effects of BK pretreatment were blocked by a B2 receptor antagonist (HOE-140; 10 microm) or a protein
18 a specific kinin B1 receptor agonist), kinin B2 receptor antagonists: HOE140 (30 micrograms kg-1 i.v.
19 (b) the ACEi ramipril, with and without the B2 receptor antagonist icatibant (B2-ant); or (c) an AT1
23 ot support clinical efficacy of a bradykinin B2 receptor antagonist in ACE inhibitor-associated angio
25 bcutaneous icatibant, a selective bradykinin B2 receptor antagonist, or to the current off-label stan
26 -Gly4-Phe5 section of the peptide bradykinin B2 receptor antagonist [Pro3, Phe5]HOE 140 (D-Arg0-Arg1-
27 h HOE-140 (0.3 mg/kg), a specific bradykinin B2-receptor antagonist, produced no significant alterati
28 ols) was completely blocked by either NK1 or B2 receptor antagonists (SR140333 or FR172357, respectiv
29 ect of B2 receptor blockade using icatibant (B2 receptor antagonist) was studied using a pressure-tar
30 ght to test the hypothesis that a bradykinin B2 receptor antagonist would shorten time-to-resolution
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