Pain hypersensitivity after tissue injury and inflammation is contributed to by a reduction in the threshold and an increase in the responsiveness of the peripheral terminals of high-threshold nociceptor neurons, the phenomenon of peripheral sensitization. Bradykinin, acting via G-protein-coupled receptors expressed by the sensory neurons, links to multiple intracellular signaling pathways that in turn interact with voltage-gated and ligand-gated ion channels, changing their properties in such a way as to enhance the response to peripheral stimuli.
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Wang et al. (2006) studied this question.