ABSTRACT
Classical inflammatory mediators such as bradykinin, serotonin, prostanoids, histamine, and low pH have been shown to activate and sensitize nociceptors with histamine being the best characterized pruritogen (Ikoma et al. 2006). There are only few mediators that can induce histamine-independent pruritus. Prostaglandins were found not only to enhance histamine-induced itch in the skin (Hägermark et al. 1977) but also to act directly as pruritogens in the conjunctiva (Woodward et al. 1995) and in human skin when applied via microdialysis fibers (Neisius et al. 2002). Acetylcholine has been identified as a pruritic in atopic dermatitis (AD) patients, whereas it induces pain in normal subjects (Heyer et al. 1997). This mechanism could probably explain the itch which many AD patients experience when they sweat. The potency of the well-established pruritics in normal skin can be defined as histamine > prostaglandin E2 > acetylcholine, serotonin (Schmelz et al. 2003b). In contrast, bradykinin and capsaicin application usually induce a pure pain sensation.
