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Effect of Angiotensin‐Converting Enzyme Inhibition on Bronchial Responsiveness
Author(s) -
Dicpinigaitis Peter V.,
Dobkin Jay B.
Publication year - 1996
Publication title -
the journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.92
H-Index - 116
eISSN - 1552-4604
pISSN - 0091-2700
DOI - 10.1002/j.1552-4604.1996.tb04213.x
Subject(s) - angiotensin converting enzyme , enzyme , pharmacology , renin–angiotensin system , angiotensin ii , chemistry , medicine , endocrinology , biochemistry , receptor , blood pressure
The effect of angiotensin‐converting enzyme (ACE) inhibition on bronchial responsiveness has not been clearly established. Because ACE degrades bradykinin and substance P, inhibition of the enzyme may lead to accumulation of these potent bronchoconstrictors in the lung, potentially leading to enhanced bronchial reactivity or bronchospasm. Previous studies of the effect of ACE inhibition on airway responsiveness have yielded conflicting results. A randomized, double‐blind, placebo‐controlled study was therefore conducted to evaluate the effect of a 14‐day course of oral lisinopril (10 mg for days 1–3, 20 mg for days 4–14) on bronchial responsiveness to inhaled methacholine in a group of healthy volunteers. No significant change in methacholine responsiveness occurred in any of the participants receiving lisinopril. The mean (±SD) concentration of methacholine producing a decrease in FEV 1 of 20% from baseline (PC 20 ; mg/mL) was 23.3 ± 5.0 before the study and 23.5 ± 4.5 at the end of the study for the lisinopril group, and 23.0 ± 4.6 before the study and 21.8 ± 6.9 after the study for the placebo group. The 14‐day course of ACE inhibitor therapy did not enhance nonspecific bronchial responsiveness in healthy volunteers.