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Louis-Philippe Boulet, MD; Joanne Milot, BSc; Noël Lampron, MD; Yves Lacourcière, MD

JAMA. 1989;261(3):413-416.

Abstract
Angiotensin-converting enzyme inhibitors sometimes cause cough; the mechanism is unknown. We therefore studied the effects of ambulatory treatment with captopril on pulmonary function and on nonspecific bronchial responsiveness to methacholine in 15 hypertensive subjects. Lung volumes, expiratory flows and nonspecific bronchial responsiveness to methacholine using doses up to 64 g/L were measured before and four and eight weeks after captopril treatment was started. Throughout the study the subjects recorded respiratory symptoms and peak expiratory flow rates. In four subjects a persistent cough developed related to the use of captopril, but this was not associated with the development of airflow obstruction or bronchial hyperresponsiveness. The mean provocative concentration of methacholine that resulted in a 20% fall in the forced expiratory volume in 1 s was 43.6 ± 1.8 g/L after eight weeks of captopril treatment compared with 61.6 ± 1.2 g/L at the baseline evaluation. We concluded that there was no significant change in lung function during treatment with captopril. The development of a cough related to this medication is not associated with the development of airflow obstruction or airway hyperresponsiveness.

(JAMA 1989;261:413-416)

Author Affiliations
From the Pulmonary Research Unit, Laval Hospital (Drs Boulet and Lampron and Ms Milot), and the Hypertension Clinic, Le Centre Hospitalier de l'Université Laval (Dr Lacourcière), Sainte-Foy, Quebec.

Footnotes
Reprint requests to Centre de Pneumologie, Hôpital Laval, 2725 Chemin Sainte-Foy, Sainte-Foy, Quebec, Canada G1V 4G5 (Dr Boulet).

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