Figure 5.

Proposed mechanism for the induction of delayed cardioprotection by bradykinin. The immediate activation of NOS as a result of bradykinin B₂ receptor activation leads to the generation of NO. The most likely NOS isoform is eNOS. According to prevailing the delayed preconditioning hypothesis, NO could subsequently trigger an adaptive response in cardiac myocytes, involving the activation of protein kinase C (PKC) isoforms and other kinases. The subsequent induction of unknown mediators of protection results in enhanced tolerance to ischaemia 24 h following liberation or application of bradykinin. Adapted from Ebrahim et al. (2001b).