Open AccessEffects of Angiotensin-Converting Enzyme Inhibitors on Spontaneous or Stimulated Generation of Reactive Oxygen Species by Bronchoalveolar Lavage Cells Harvested From Patients With or Without Chronic Obstructive Pulmonary Disease.
Author(s) -
Shinji Teramoto,
Masashi Suzuki,
Takeshi Matsuse,
Takeo Ishii,
Yoshinosuke Fukuchi,
Yasuyoshi Ouchi
Publication year - 2000
Publication title -
japanese journal of pharmacology/japanese journal of pharmacology
Language(s) - English
Resource type - Journals
eISSN - 1347-3506
pISSN - 0021-5198
DOI - 10.1254/jjp.83.56
Subject(s) - bronchoalveolar lavage , copd , reactive oxygen species , lisinopril , angiotensin converting enzyme , medicine , ace inhibitor , pharmacology , ambroxol , chemistry , immunology , endocrinology , biochemistry , lung , anesthesia , blood pressure
We examined the effects of angiotensin-converting enzyme (ACE) inhibitors on spontaneous or stimulated generation of reactive oxygen species (ROS) by bronchoalveolar lavage (BAL) cells prepared from 6 patients with chronic obstructive pulmonary disease (COPD) and from age-matched control subjects without COPD. The ROS produced by BAL cells were measured by the lucigenin-dependent chemiluminescence method. The application of ACE inhibitors into culture media containing BAL cells inhibited spontaneous and stimulated generation of ROS by BAL cells from COPD patients and control subjects in an ambroxol-concentration-dependent manner. Alacepril, an ACE inhibitor bearing SH-group, inhibited the oxygen radical production and generation by BAL cells from COPD patients in a dose-dependent fashion. Approximately 0.6-0.7 mM of alacepril inhibited 50% of the ROS production by BAL cells from COPD patients, whereas a slightly higher concentration (3 mM) of lisinopril, an ACE inhibitor not bearing an SH-group, was necessary to inhibit the production of ROS. These results suggest that an ACE inhibitor may act as an pulmonary antioxidant in patients with COPD.