Table of Contents Author Guidelines Submit a Manuscript
Canadian Respiratory Journal
Volume 1, Issue 4, Pages 235-240
http://dx.doi.org/10.1155/1994/519168
Basic Research

Captopril-Associated Cough Is Not due to Increased Airway Responsiveness

SP Blackie, C Hilliam, R Porter, R Rangno, and PD Paré

Divisions of Respira tory Medicine and Clinical Pharmacology, University of British Columbia, Pulmonary Research Laboratory, St Paul's Hospital, Vancouver, British Columbia, Canada

Copyright © 1994 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors commonly cause cough. There is controversy as to whether preexisting airway hyperresponsivencss predisposes patients to ACE inhibitor-induced cough and whether ACE inhibitor therapy can cause airway hypcrresponsiveness.

OBJECTIVES: To lest the predictive value of baseline airway responsiveness fur the development of cough induced by ACE inhibitors, and whether patients who developed cough during ACE inhibitor therapy showed an increase in airway responsiveness.

METHODS: Baseline spiromctry and airway responsiveness to methacholinc (expressed as the concentrat ion of mcthacholine required to cause a 10% fall in forced expired volume in 1 s [ FEV1 or PC10) were measured in 23 hypertensive patients before and after 10 to l 2 weeks of treatment with captopril at an initial daily dose of 50 mg.

RESULTS: During caplopril therapy seven (30%) patients developed new cough, which resolved after discontinuation of captopril. The base line PC10 was the same in coughers and noncoughers and did not predict the development of cough. During caplopril therapy there was a nonsignificant decrease in the geometric mean PC10 for all patients from 15 mg/mL (range 0.8 to 62) to 13 mg/ml (range 0.7 to 62) (P=0.08). These changes were not different in cougher, and noncoughers. FEV1, forced vital capacity and total lung capacity did not change during the study.

CONCLUSIONS: Cough caused by captopril is not predicted by baseline airway responsiveness and is not associated with increased airway res ponsiveness