Peripheral sensory nerve endings involved in the cough reflex

Peripheral sensory nerve endings involved in the cough reflex are the primary afferent terminals of the vagus nerve, specifically Aδ-fibers and C-fibers, located within the airway mucosa, larynx, and lungs (NIH, 2011; NIH, 2023). These nerve endings function as sensors that detect mechanical and chemical irritants—such as dust, mucus, or inflammatory mediators—and transmit signals to the cough center in the brainstem to initiate the cough reflex (NIH, 2017; ResearchGate, 2023). They express a variety of molecular targets, including voltage-gated sodium channels (e.g., Nav1.7), P2X3 purinergic receptors, and transient receptor potential (TRP) channels like TRPV1 and TRPA1 (NIH, 2020; ResearchGate, 2023). In conditions such as chronic cough, asthma, and COPD, these nerve endings can become hypersensitive, a state known as cough hypersensitivity syndrome, leading to excessive coughing in response to low-level stimuli (NIH, 2020). Therapeutic strategies involve desensitizing or anesthetizing these endings to reduce the urge to cough; for example, benzonatate acts by inhibiting stretch receptors and sodium channels on these fibers, while newer agents like gefapixant target specific P2X3 receptors to reduce nerve firing (StatPearls, 2023; NIH, 2020).

Other names

Vagal afferent nerve endingsAirway sensory nerve endingsPulmonary stretch receptorsCough receptorsBronchopulmonary sensory nerves

Drugs targeting these nerve endings act by inhibiting the initiation or conduction of sensory impulses. This is achieved through various mechanisms, including the blockade of voltage-gated sodium channels (e.g., benzonatate, lidocaine), antagonism of P2X3 purinergic receptors (e.g., gefapixant), or desensitization of transient receptor potential (TRP) channels (e.g., capsaicin) (NIH, 2011; NIH, 2020).