Neurogenic inflammation and pancreatitis.
Stimulation of primary sensory neurons produces local vasodilation, plasma extravasation, and pain and is due largely to the release of the tachykinins substance P and calcitonin-gene-related peptide. Pathological activation of sensory neurons and the inflammatory sequelae are known as neurogenic inflammation and appear to be important in many organ systems, including the pancreas. Factors that stimulate primary sensory neurons include hydrogen ions, heat, leukotrienes, arachidonic acid metabolites, bradykinin, and proteases such as trypsin, all of which may participate in the generation of acute pancreatitis. The current review examines the cellular and molecular mechanisms involved in sensory nerve activation within the pancreas and the potential contribution of neurogenic inflammation to the pathogenesis of pancreatitis.
Liddle
Rodger A
RA
Department of Medicine, Duke University, and Durham VA Medical Centers, Durham, NC 27710, USA. liddl001@mc.duke.edu
Nathan
Jaimie D
JD
D001920:Bradykinin / Q000502:physiology; D006801:Humans; D007473:Ion Channels / Q000502:physiology; D020078:Neurogenic Inflammation / Q000209:etiology*; D009475:Neurons, Afferent / Q000502:physiology; D010195:Pancreatitis / Q000503:physiopathology*; D011955:Receptors, Drug / Q000502:physiology; D013373:Substance P / Q000502:physiology; D050916:TRPV Cation Channels
D007473:Ion Channels; D011955:Receptors, Drug; D050916:TRPV Cation Channels; C494482:TRPV1 protein, human; D013373:Substance P; D001920:Bradykinin