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Cough accompanied by an increased sensitivity of the cough reflex is the most common symptom of inflammatory airway disease^1,5. This symptom is also frequently reported in patients receiving angiotensin–converting enzyme (ACE) inhibitors as therapy for heart failure or hypertension^2–4, although the underlying mechanism is unknown. We have investigated the possibility that the inflammatory peptide bradykinin, normally degraded by ACE, causes sensitization of airway sensory nerves and an enhancement of the cough reflex in conscious guinea pigs. Treatment of guinea pigs for two weeks with captopril led to an increased cough response to inhaled citric acid, which was prevented by concomitant treatment with the bradykinin receptor antagonist icatibant. A similar icatibant–sensitive enhancement of citric acid–evoked cough was seen in untreated animals after prior inhalation of bradykinin, although cough …