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The Positive Association of Cough with Angiotensin‐Converting Enzyme Inhibitors
Author(s) -
Just Paul M.
Publication year - 1989
Publication title -
pharmacotherapy: the journal of human pharmacology and drug therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.227
H-Index - 109
eISSN - 1875-9114
pISSN - 0277-0008
DOI - 10.1002/j.1875-9114.1989.tb04107.x
Subject(s) - ramipril , captopril , medicine , lisinopril , enalapril , angiotensin converting enzyme , cough reflex , ace inhibitor , stimulation , pharmacology , provocation test , reflex , anesthesia , blood pressure , pathology , alternative medicine
Captopril, enalapril, lisinopril, ramipril, cilazipril, and quinipril have all been documented to induce cough with an estimated frequency of at least 15% of treated patients. Common descriptors include tickling, dry, nonproductive, and persistent. Onset usually occurs during the first week of therapy and lasts as long as the drug is taken, remitting within a few days after the agent is discontinued. Alternative angiogensin‐converting enzyme (ACE) inhibitors replicate the cough. The mechanism seems related to stimulation of lung afferent C fibers, perhaps by prostaglandin E 2 . It may also be related to decreased breakdown of substance P, the neurochemical mediator of the cough reflex released in response to stimulation of C fibers and metabolized by ACE. The possible role of prostaglandins is supported by two anecdotal reports of cough disappearing in patients receiving nonsteroidal antiinflammatory agents. Future trials should recognize cough as a side effect of ACE inhibitor therapy, and prospective determination of its true frequency and cross‐occurrence are necessary.