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Original Research: COPD |

Effects of Aerosolized Adenosine 5′-Triphosphate in Smokers and Patients With COPDAdenosine 52032-Triphosphate in COPD

Ozen K. Basoglu, MD; Peter J. Barnes, DM, DSc, Master FCCP; Sergei A. Kharitonov, MD; Amir Pelleg, PhD
Author and Funding Information

From the Department of Chest Diseases (Dr Basoglu), Ege University School of Medicine, Izmir, Turkey; the Airway Disease Section (Drs Barnes and Kharitonov), National Heart & Lung Institute, Imperial College, London, England; and the Department of Medicine (Dr Pelleg), Drexel University College of Medicine, Philadelphia, PA.

CORRESPONDENCE TO: Amir Pelleg, PhD, Drexel University College of Medicine, Department of Medicine, NCB Mail Box 470, 245 N 15th St, Philadelphia, PA 19102-1192; e-mail: apelleg@drexelmed.edu


FUNDING/SUPPORT: The authors have reported to CHEST that no funding was received for this study.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians. See online for more details.


Chest. 2015;148(2):430-435. doi:10.1378/chest.14-2285
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BACKGROUND:  Extracellular adenosine 5′-triphosphate (ATP) stimulates vagal C and Aδ fibers in the lung, resulting in pronounced bronchoconstriction and cough mediated by P2X2/3 receptors located on vagal sensory nerve terminals. We investigated the effects of nebulized ATP on cough and symptoms in control subjects, healthy smokers, and patients with COPD and compared these responses to the effects of inhaled adenosine, the metabolite of ATP.

METHODS:  We studied the effects of inhaled ATP and adenosine monophosphate (AMP) on airway caliber, perception of dyspnea assessed by the Borg score, cough sensitivity, and ATP in exhaled breath condensate in healthy nonsmokers (n = 10), healthy smokers (n = 14), and patients with COPD (n = 7).

RESULTS:  In comparison with healthy subjects, ATP induced more dyspnea, cough, and throat irritation in smokers and patients with COPD, and the effects of ATP were more pronounced than those of AMP. The concentration of ATP in the exhaled breath condensate of patients with COPD was elevated compared with that of healthy subjects.

CONCLUSIONS:  Smokers and patients with COPD manifest hypersensitivity to extracellular ATP, which may play a mechanistic role in COPD.

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