Every tissue that is susceptible to inflammation is innervated by nerves containing neurotransmitters, which can mediate or modulate each component of an inflammatory response. The sensation of pain and the obligatory role of nerves in this key component of inflammation provide indisputable evidence that neuronal activation is a necessary condition for inflammatory disease. The pioneering studies of Bruce I and Lewis 2, 3 and the more recent studies of Jansco et al. 4 and others 5, 6 reveal that neuronal activation might also be the defining event in an inflammatory response. These facts make it difficult to discount the role of the nervous system when studying the mechanisms of inflammation associated with any tissue, organ, o r disease. Tachykinins are neuropeptides found in nerve endings throughout the skin, mucosa, and viscera where they act as potent mediators of vasodilatation, plasma extravasation, inflammatory cell recruitment, and pain. 6-11 Because these neuropeptides are released from the central and peripheral terminations of afferent nerves in response to many mechanical and chemical stimuli, 57 it seems likely that tachykinins contribute to the pathophysiology and symptoms of inflammatory disease. Consequently, drugs that antagonize the actions of these neuropeptides might be useful for treating the clinical
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Brendan J. Canning (1997) studied this question.
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