Effect of angiotensin-converting enzyme inhibition on bronchial responsiveness

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Abstract

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 FEV1 of 20% from baseline (PC20; 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.

Original languageEnglish (US)
Pages (from-to)361-364
Number of pages4
JournalJournal of Clinical Pharmacology
Volume36
Issue number4
StatePublished - Apr 1996

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Lisinopril
Methacholine Chloride
Peptidyl-Dipeptidase A
Healthy Volunteers
Placebos
Bronchoconstrictor Agents
Enzyme Therapy
Bronchial Spasm
Bradykinin
Substance P
Angiotensin-Converting Enzyme Inhibitors
Lung
Enzymes

ASJC Scopus subject areas

  • Pharmacology (medical)
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

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title = "Effect of angiotensin-converting enzyme inhibition on bronchial responsiveness",
abstract = "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 FEV1 of 20{\%} from baseline (PC20; 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.",
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N2 - 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 FEV1 of 20% from baseline (PC20; 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.

AB - 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 FEV1 of 20% from baseline (PC20; 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.

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