• Marian Kollarik, Fei Ru, and Bradley J Undem.
• The Johns Hopkins School of Medicine, Johns Hopkins Asthma and Allergy Center, Baltimore, MD 21224, USA. kollarik@jhmi.edu
• Pulm Pharmacol Ther. 2007 Jan 1;20(4):402-11.

AbstractAcid is an important mediator in the pathogenesis of cough. Inhalation of exogenous acid triggers cough and endogenous acid may contribute to cough in respiratory diseases. Acid directly stimulates vagal bronchopulmonary sensory nerves that regulate the cough reflex. Consistent with their putative role in defence against aspiration and inhaled irritants, Adelta-fibre nociceptors in the large airways are most efficiently stimulated by rapid acidification. In contrast, acid-sensitive properties of the C-fibre nociceptors allow for continuous monitoring of pH which is likely important in inflammation. Acid is also the single most important mediator in the pathogenesis of cough due to gastro-oesophageal reflux (GOR). The cough pathways can be sensitized by the sensory inputs from the oesophagus. This sensitization is likely mediated by a subset of the vagal oesophageal sensory nerves distinguished by discriminative responsiveness to noxious stimuli (nociceptors). The receptors underlying acid sensitivity of vagal sensory nerves are incompletely understood. The role of TRPV1 has been established but the roles of acid-sensing ion channels (ASIC) and other receptors await more definitive investigation. Here, we provide a brief overview of the cough-related acid-sensitive sensory pathways and discuss the mechanisms of acid sensitivity.

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