Non-genomic mechanism of corticosterone inhibition of bradykinin-induced calcium influx in PC12 cells: Involvement of protein kinase C

Bradykinin (BK) induces an increase in [Ca²⁺]₁ via intracellular Ca²⁺ release and extracellular Ca²⁺ influx through the transduction of G protein, but not through voltaged-sensitive calcium channels, the actions of BK can be rapidly inhibited by corticosterone (B). In this experiment. We analysed how B influences bradykinin (BK)-induced intracellular Ca²⁺ release and extracellular Ca²⁺ influx, and further studied the mechanism of the rapid action of corticosterone. To dissociate the intracellular Ca²⁺ release and extracellular Ca²⁺ influx induced by BK, the Ca²⁺- free/Ca²⁺-reintroduction protocol was used. The results were as follows: (1) The Ca²⁺ influx induced by BK could be rapidly inhibited by B, but intracellular Ca²⁺ release could not be affected significantly. (2) The inhibitory effect of B-BSA (bovine serum albumin-conjugated corticosterone) on Ca²⁺ influx induced by BK was the same as the effect of free B. (3) PKC activator (PMA) could mimic and PKC inhibitor Go6976 could reverse the inhibitory effect of B. (4) There was no inhibitory effect of B on Ca²⁺ influx induced by BK when pretreated with PTX. The results suggested that B might act via its putative membrane receptor and inhibit the Ca²⁺ influx induced by BK through the PTX-sensitive G protein-PKC pathway.