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Role of bradykinin in the vascular permeability response induced by carrageenin in rats
Author(s) -
Kumakura Seiichiro,
Kamo Izumi,
Tsurufuji Susumu
Publication year - 1988
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.1476-5381.1988.tb11457.x
Subject(s) - bradykinin , medicine , endocrinology , vascular permeability , chemistry , captopril , kunitz sti protease inhibitor , permeability (electromagnetism) , trypsin , enzyme , biochemistry , receptor , membrane , blood pressure
1 Bradykinin in carrageenin‐induced inflammatory pouch fluid was measured by an enzyme immunoassay method. 2 The bradykinin showed a single peak in the 30–60 min period after the challenge and then decreased quickly, and there was a correlation between the bradykinin level and exudation of fluorescein‐labelled bovine serum albumin in the first 60 min period. 3 Captopril (an inhibitor of kininase II) elevated both the bradykinin level in the inflammatory pouch fluid and vascular permeability, while dl ‐2‐mercaptomethyl‐3‐ guanidinoethylthiopropanoic acid (an inhibitor of kininase I) had no effect. 4 Soybean trypsin inhibitor (SBTI) inhibited the vascular permeability response in parallel with the decrease in the bradykinin level. 5 A bradykinin‐degrading activity appeared in the pouch fluid within 1 h after the challenge and increased with time. 6 In the period of 3.5–4 h, bradykinin levels were suppressed below the sensitivity limit of the assay, i.e. 0.07 ng ml −1 , in spite of active generation. This was because degradation of bradykinin was very rapid in this late stage. Nevertheless, bradykinin still played a definite role in sustaining a high level of vascular permeability response in the late stage in conjunction with prostaglandins.