作者: Gábor Pethő , Peter W. Reeh
DOI: 10.1016/S1567-7443(08)10407-0
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摘要: Abstract Bradykinin is a potent mediator formed upon tissue damage and inflammation. It can both excite sensitize nociceptors to heat, mechanical, chemical stimuli. Two types of bradykinin receptors (B1 B2) have been identified which the constitutive B2 mediate most acute effects in uninflamed tissues while B1 are induced become activated during Both receptor subtypes utilize similar signaling pathways including activation protein kinase C (PKC), elevation intracellular Ca2+ concentration, release arachidonic acid. PKC major mechanism underlying neuronal excitatory heat-sensitizing actions accumulation induces formation nitric oxide within sensory neurons involved – together with downregulation development tachyphylaxis receptor-mediated bradykinin. Nitric oxide, however, may also contribute sensitizing Cyclooxygenase metabolites acid (prostanoids) be Recently, new has revealed for involves capsaicin TRPV1 through 12-lipoxygenase products According novel hypothesis, action not separate effect but fact heat response as result massive sensitization threshold drop below ambient temperature. Prostanoids stimuli predominantly via cyclic adenosine 3′,5′-monophosphate–protein A pathway that modulates various membrane channels Ca2+-dependent or voltage-gated K+ channels, tetrodotoxin-resistant Na+ well ligand-gated noxious heat-gated ion channels.