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The effects of intradermal bradykinin are potentiated by angiotensin converting enzyme inhibitors in hypertensive patients.
Author(s) -
Ferner RE,
Wilson D.,
Paterson J.R.,
Wilkinson R.,
Rawlins MD
Publication year - 1989
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1989.tb05374.x
Subject(s) - bradykinin , captopril , enalapril , angiotensin converting enzyme , medicine , ace inhibitor , enzyme inhibitor , pharmacology , adverse effect , endocrinology , enzyme , receptor , blood pressure , chemistry , biochemistry
1. To test the hypothesis that angiotensin converting enzyme (ACE) inhibitors potentiate the tissue effects of bradykinin, the thickness of weals produced by intradermal injections of bradykinin was measured in 17 hypertensive subjects whose antihypertensive regimen included an ACE inhibitor, and in 12 whose treatment did not. 2. Weal thickness increased linearly with the logarithm of the bradykinin dose in both groups (P less than 0.0001). 3. The patients receiving ACE inhibitors showed a mean response of 1.18 +/‐ 0.08 mm (mean +/‐ s.e. mean), compared with a mean response of 0.75 +/‐ 0.08 mm for patients not receiving an ACE inhibitor (P = 0.002). Mean weal response (1.08 +/‐ 0.9 mm) was not significantly different in patients taking captopril (n = 11) compared with that (1.29 +/‐ 0.12 mm) in patients taking enalapril (n = 9). 4. Facial flushing during the experiment occurred in six patients taking ACE inhibitors but none who were not. 5. Dermal responses to bradykinin are enhanced in patients taking ACE inhibitors as routine antihypertensive therapy. This study supports the hypothesis that bradykinin may be responsible for some of the adverse effects of these drugs.