Lung
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Sneezing, cough, mucus secretion, and bronchoconstriction represent the main components of a coordinated and efficient reaction direct to expel or neutralize irritant agents from the respiratory system. A dense network of sensory nerves localized from the nose to the lower airways beneath the epithelium subserves this function. A variety of receptors and channels present in sensory nerve terminals by sensing irritant stimuli activate the system in emergence and initiate protective reflex responses, including cough. Previous and recent literature highlights the prominent role of some transient receptor potential (TRP) ion channels, and specifically the vanilloid 1 (TRPV1) and the ankyrin 1 (TRPA1) as sensors of airway irritation and initiators of the cough reflex.
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In healthy nonsmokers, inhalation of one single puff of cigarette smoke immediately evoked airway irritation and cough, which were either prevented or markedly diminished after premedication with hexamethonium. Single-fiber recording experiments performed in anesthetized animals showed that both C fibers and rapidly adapting receptors in the lungs and airways were stimulated by inhalation of one breath of cigarette smoke. Application of nicotine evoked an inward current and triggered depolarization and action potentials in a concentration-dependent manner in a subset of isolated vagal pulmonary sensory neurons. ⋯ In contrast to the observations in animal studies, both enhanced and diminished cough sensitivities to tussive agents have been reported in chronic smokers. This discrepancy is probably related to the history of chronic smoking of the individual smokers and the severity of existing airway inflammation and dysfunction. Furthermore, several other factors possibly contributing to the regulation of cough receptor sensitivity in chronic smokers should also be considered.