Bronchopulmonary C-fibers and acid-sensitive, capsaicin-insensitive mechanoreceptors innervating the larynx, trachea and large bronchi regulate the cough reflex. These vagal afferent nerves may interact centrally with sensory input arising from afferent nerves innervating the intrapulmonary airways or even extrapulmonary afferents such as those innervating the nasal mucosa and esophagus to produce chronic cough or enhanced cough responsiveness. The mechanisms of cough initiation in health and in disease are briefly described.
Keywordscapsaicin; vagal; bradykinin; NMDA The cough reflex protects the airways and lungs from aspiration, inhaled irritants, particulates and pathogens and clears the air spaces of accumulated secretions. Studies in animals provide conclusive evidence that cough is initiated by activation of vagal afferent nerves. Precisely which afferent nerve subtypes regulate cough has been debated and reviewed elsewhere [1]. In this review, we describe the stimuli that initiate cough and the mechanisms by which these stimuli activate airway sensory nerves. These data are related to the known physiological properties of bronchopulmonary afferent nerve subtypes. The review concludes with a discussion of the potential interactions between afferent nerve subtypes and the possible mechanisms of altered cough reflexes in disease.
Chemical and Mechanical Stimuli That Initiate CoughingMultiple chemical and mechanical stimuli have been shown to initiate coughing in human subjects and in animals [1][2][3][4]. Several of these stimuli, including capsaicin, citric acid, hypertonic saline and low chloride buffers/ solutions, are often used to evoke cough experimentally. Other stimuli known to initiate coughing in animals and in human subjects include particulate/ dust, mechanical/ vibratory stimulation of the airway mucosa larynx or chest wall, chemical irritants such as resiniferetoxin, cinnamaldehyde and allylisothiocyanate (AITC), and the autacoids bradykinin, anandamide and prostaglandin E2 (PGE2). Although