Abstract
Bradykinin caused graded contraction in the guinea pig ileum, trachea and urinary bladder and rat uterus and vas deferens in vitro. The order of potency (EC 50, nM) was: ileum (3) > uterus (5) > trachea (15) > vas deferens (41) > urinary bladder (52) and the maximal responses (percentage to 80 mM KCl) were: 152 ± 8 (ileum), 122 ± 6 (uterus), 97 ± 3 (urinary bladder), 75 ± 5 (trachea) and 33 ± 3 (vas deferens). Responses to bradykinin in guinea pig ileum and urinary bladder and rat vas deferens and uterus were markedly attenuated in Ca 2+-free medium with or without EGTA or by nicardipine, whereas those in guinea pig trachea depended almost exclusively on intracellular Ca 2+ sources which were sensitive to ryanodine. Treatment of the animals with pertussis toxin only inhibited bradykinin-induced contraction of the rat uterus. Furthermore, the protein kinase C inhibitors, H 7 (5-isoquinolinysulfonyl-2-methyl-piperazine) and staurosporine, antagonized in a graded manner bradykinin responses in guinea pig ileum and trachea and rat vas deferens, indicating the possible dependence on activation of protein kinase C mechanisms, while responses of the rat uterus rely on coupling by a pertussis toxin-sensitive G protein. Thus, bradykinin acting at B 2 receptors may induce contractions in several smooth muscles from rat and guinea pig through activation of multiple second messenger pathways.
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