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[Leu 8 ]des‐Arg 9 ‐bradykinin inhibits the angiogenic effect of bradykinin and interleukin‐1 in rats
Author(s) -
Hu DeEn,
Fan TaiPing D.
Publication year - 1993
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1993.tb13525.x
Subject(s) - bradykinin , endocrinology , neovascularization , receptor antagonist , medicine , angiogenesis , receptor , chemistry , antagonist , pharmacology
1 Subcutaneous implantation of sterile polyether sponges in rats elicited a reproducible neovascular response over 14 days, as determined by measurements of relative sponge blood flow by a 133 Xe clearance technique. The angiogenic response was verified by quantitation of haemoglobin contents and histological evaluation of vascularized sponges. 2 Daily administration of 1 nmol of bradykinin (BK) into the implants significantly enhanced the basal sponge‐induced neovascularization, leading to higher 133 Xe clearance values, increased haemoglobin contents, cellularity and vascularity. 3 When given alone, lower doses of BK (10 pmol) or recombinant human interleukin‐1 α (IL‐1α, 0.3 pmol) produced no apparent effects on the basal sponge‐induced angiogenesis. However, co‐administration of these two peptides produced an angiogenic response similar to that elicited by 1 nmol of BK. 4 The BK/IL‐1α‐induced neovascularization was abolished by the bradykinin B 1 receptor antagonist, [Leu 8 ]des‐Arg 9 ‐BK (1 nmol day −1 ), but not by the B 2 receptor antagonist Ac‐ d ‐Arg‐[Hyp 3 , d ‐Phe 7 ,Leu 8 ]‐BK (1 nmol day −1 ). 5 Thus, if such interaction between BK and IL‐1α contributes to the excessive neovascularization in chronic inflammatory diseases, the blockade of B 1 receptors may provide an effective treatment.