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Regulation of bradykinin receptor level by cholera toxin, pertussis toxin and forskolin in cultured human fibroblasts
Author(s) -
Etscheid Beth G.,
Ko Peter H.,
Villereal Mitchell L.
Publication year - 1991
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.1476-5381.1991.tb09791.x
Subject(s) - cholera toxin , forskolin , pertussis toxin , bradykinin , arachidonic acid , cycloheximide , toxin , biology , receptor , endocrinology , medicine , microbiology and biotechnology , chemistry , biochemistry , g protein , enzyme , protein biosynthesis
1 The effect of bacterial toxins on bradykinin‐triggered release of arachidonic acid was studied in serum‐deprived human foreskin (HSWP) fibroblasts prelabelled with [ 3 H]‐arachidonic acid. An 18‐h exposure of HSWP cells to cholera toxin, pertussis toxin, or forskolin enhanced the bradykinin‐stimulated release of arachidonic acid and metabolites. 2 Prolonged treatment of HSWP cells with these agents also caused a 3 to 4 fold rise in cell surface [ 3 H]‐bradykinin binding. The rise was inhibited by concurrent incubation with cycloheximide or actinomycin D. In addition, cholera toxin and foreskolin increased [ 3 H]‐bradykinin binding in wildtype PC12 cells, but not in mutant PC12 cells with reduced cyclic AMP‐dependent protein kinase type II activity. 3 In conclusion, cholera toxin, pertussis toxin and forskolin enhanced arachidonic acid release in response to bradykinin, and increased the number of bradykinin receptors in HSWP fibroblasts. A cyclic AMP‐dependent mechanism appears to mediate the actions of the toxins and forskolin.