The human
cough reflex is still poorly understood, although it is known to occur independently of bronchoconstriction. Sensitization of the
cough reflex is a unifying hypothesis for chronic dry
cough in several conditions, including gastroesophageal
acid reflux,
angiotensin-converting enzyme inhibitor cough, and
cough-variant asthma. The most common cause of chronic dry
cough is a group of related conditions of chronic
rhinitis,
sinusitis, and postnasal drip. In these cases the
cough reflex may be sensitized through an action of inflammatory mediators from the nasal mucosa on the airways or a reflex sensitization of airway sensory nerves. The association of
cough with
gastroesophageal reflux may occur through a local esophageal-tracheobronchial reflex.
Angiotensin-converting enzyme inhibitor cough is a side effect of treatment in about 10% of patients; it probably results from inhibition of the degradation of
kinins, particularly
bradykinin, in the airway. Why some patients with
asthma have
cough as the principal feature of their disease is unclear.
Tachykinins are probably involved in the mechanism of sensitization of the
cough reflex, and the development of
neuropeptide antagonists may open new research opportunities. A study that used ambulatory recording of
cough in a group of subjects with
asthma confirmed the presence of significant
cough, the frequency of which did not correlate with lung function or diurnal variation in peak flow. This finding highlights the problem of
cough in patients with
asthma, a problem that probably has been underestimated in the past.