ABSTRACT
The cough reflex is subserved by vagal primary afferent nerves such as
bronchopulmonary rapidly adapting receptors (RARs) which can be stimulated by mechanical stimulation and deformation of the airway epithelium,
such as by particulate matter or mucus, and by airway smooth muscle
contraction induced by constrictor agents (1,2). These are predominantly
present in the larynx, trachea, and carina. Activation of bronchopulmonary
C-fibers by chemicals such as bradykinin and capsaicin can also evoke
cough (3,4), although these may also activate the RARs. Peptide neuro-
transmitters are often associated with capsaicin-sensitive afferent C-fibers
in the airways. In rodents, stimulation of C-fibers initiates local axonal reflexes mediated by the release of neuropeptides such as neurokinin A
and substance P which may also induce cough indirectly by causing edema,
mucus secretion, and airway smooth muscle contraction. These in turn can
stimulate RARs. Pulmonary C-fibers may also inhibit RAR fiber activity.
