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Pulmonary function and airway responsiveness during long-term therapy with captopril
L P Boulet1, J Milot, N Lampron
1Pulmonary Research Unit, Laval Hospital, Sainte-Foy, Quebec, Canada.
JAMA
|January 20, 1989
Summary
Angiotensin-converting enzyme inhibitors like captopril may cause cough. This study found that captopril-induced cough in hypertensive patients is not linked to lung function changes or increased airway hyperresponsiveness.
Area of Science:
- Pulmonary Medicine
- Pharmacology
Background:
- Angiotensin-converting enzyme (ACE) inhibitors are frequently prescribed for hypertension.
- Cough is a common side effect of ACE inhibitors, but its underlying mechanism remains unclear.
- The relationship between ACE inhibitor-induced cough and pulmonary function changes requires further investigation.
Purpose of the Study:
- To investigate the effects of captopril on pulmonary function and bronchial responsiveness in hypertensive patients.
- To determine if captopril-induced cough is associated with airflow obstruction or increased airway hyperresponsiveness.
Main Methods:
- A study involving 15 hypertensive subjects treated with captopril.
- Measurements of lung volumes, expiratory flows, and bronchial responsiveness to methacholine were taken before and after eight weeks of treatment.
- Subjects self-recorded respiratory symptoms and peak expiratory flow rates throughout the study.
Main Results:
- Four subjects developed a persistent cough attributed to captopril.
- No significant changes in lung function (lung volumes, expiratory flows) were observed during captopril treatment.
- The mean provocative concentration of methacholine causing a 20% fall in forced expiratory volume in 1 second (FEV1) showed a trend towards a lower value after treatment, but the cough was not associated with airflow obstruction or hyperresponsiveness.
Conclusions:
- Ambulatory treatment with captopril does not significantly alter lung function in hypertensive patients.
- The development of cough associated with captopril use is not linked to the onset of airflow obstruction or bronchial hyperresponsiveness.