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.
Neural Plasticity Research Group, Department of Anesthesia and Critical Care, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.
Haibin
H
Wang
Corina
C
Ehnert
Gary J
GJ
Brenner
Clifford J
CJ
Woolf
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