Bradykinin and peripheral sensitization.
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.
Wang
Haibin
H
Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.
Ehnert
Corina
C
Brenner
Gary J
GJ
Woolf
Clifford J
CJ
D000818:Animals; D001920:Bradykinin / Q000502:physiology*; D006801:Humans; D006930:Hyperalgesia / Q000209:etiology*; D009619:Nociceptors / Q000502:physiology*; D010146:Pain / Q000209:etiology*; D017933:Peripheral Nervous System / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology; D050994:Voltage-Dependent Anion Channels / Q000502:physiology
D050994:Voltage-Dependent Anion Channels; D001920:Bradykinin