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Joseph V. Levy, PhD
Pacific Presbyterian Medical Center San Francisco, Calif

JAMA. 1989;262(1):29.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

To the Editor. —

I believe that the conclusions reached by Boulet and colleagues¹ regarding airway responsiveness during 4- to 8-week therapy with captopril require some scrutiny. The authors designed their study to assess airway responsiveness and reactivity in hypertensive patients using a provocative concentration of the cholinergic agonist methacholine. Based on their results, they conclude that the development of cough related to captopril use is not associated with the "development of airway hyperresponsiveness."

These conclusions must be interpreted more narrowly since the authors evaluated the reactivity to methacholine only and not other substances and mediators more likely to be implicated as causative factors in cough induced by angiotensin-convertive enzyme (ACE) inhibitors. Specifically, there is experimental and clinical evidence that captopril may prevent the catabolism of bradykinin, a peptide that is a potent bronchoconstrictor, as well as being able to provoke cough that mimics that caused by captopril and . . . [Full Text PDF of this Article]

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