We studied the effects of angiotensin converting enzyme (ACE) inhibitors on cough responses to bradykinin (BK), substance P (SP) and citric acid in a double blind, random study on 10 hypertensive patients receiving ACE inhibitors. Of these patients, five had reported cough with ACE inhibitors. Cough responses to citric acid were similar between patients with and without cough, and SP up to 10-5 M did not cause cough in any of the subjects. BK caused cough at 13.4 ± 1.2 (-log M) in 5 patients with cough associated with ACE inhibitors, but it did not cause cough at concentrations up to 10-5 M in other 5 patients. One month after the withdrawal of ACE inhibitors, 5 patients were free from cough symptoms, and BK did not cause cough up to 10-5 M in these patients, except for one who coughed at 10-9 M, without changes in responses to citric acid. BK caused cough at 14.3+0.7 (-log M) although BK1_7i a major metabolite of BK by ACE, caused cough at 5.7±0.7 (-log M) in another 3 patients with cough associated with ACE inhibitor. These results suggest that impaired metabolism of BK induced by ACE inhibitors may relate to the manifestation of cough in hypertensive patients receiving ACE inhibitors.bradykinin ; ACE inhibitor ; dry cough ; hypertension Angiotensin converting enzyme (ACE) inhibitors, such as captopril and enalapril have been widely used in the treatment of systemic hypertension. However, persistent dry coughs have been often reported in hypertensive patients who have been treated with ACE inhibitors (Sesoko and
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