Mechanism of Cough With Angiotensin-Converting Enzyme Inhibition

To the Editor. —Sesoko and Kaneko, 1 in the August 1985 issue of theArchives, described a patient in whom a dry cough developed during treatment with low-dose captopril. In the absence of a known mechanism, I wish to propose the hypothesis that cough results from elevated levels of bradykinin causing stimulation of small diameter sensory afferents in the lungs (type J receptors). Angiotensin-converting enzyme has been shown to be involved in the destruction of bradykinin in addition to its effects on angiotensin. 2 Inhibition of angiotensin-converting enzyme would, therefore, increase levels of bradykinin, and, in animals, this agent is known to stimulate type J receptors. 3 Excitation of these receptors may cause nonproductive cough, 4 and this is consistent with the reported effects of bradykinin when inhaled by human subjects. 5 Recently, we have described how local anesthetics may be administered as an aerosol with a particle size in