Skip to main content
British Journal of Clinical Pharmacology logoLink to British Journal of Clinical Pharmacology
. 1989 Mar;27(3):337–342. doi: 10.1111/j.1365-2125.1989.tb05374.x

The effects of intradermal bradykinin are potentiated by angiotensin converting enzyme inhibitors in hypertensive patients.

R E Ferner 1, D Wilson 1, J R Paterson 1, R Wilkinson 1, M D Rawlins 1
PMCID: PMC1379832  PMID: 2541753

Abstract

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.

Full text

PDF
337

Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Cook J., Shuster S. Histamine weal formation and absorption in man. Br J Pharmacol. 1980 Aug;69(4):579–585. doi: 10.1111/j.1476-5381.1980.tb07907.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  2. Dixon C. M., Fuller R. W., Barnes P. J. The effect of an angiotensin converting enzyme inhibitor, ramipril, on bronchial responses to inhaled histamine and bradykinin in asthmatic subjects. Br J Clin Pharmacol. 1987 Jan;23(1):91–93. doi: 10.1111/j.1365-2125.1987.tb03015.x. [DOI] [PMC free article] [PubMed] [Google Scholar]
  3. Ferner R. E., Simpson J. M., Rawlins M. D. Effects of intradermal bradykinin after inhibition of angiotensin converting enzyme. Br Med J (Clin Res Ed) 1987 May 2;294(6580):1119–1120. doi: 10.1136/bmj.294.6580.1119. [DOI] [PMC free article] [PubMed] [Google Scholar]
  4. Kiowski W., van Brummelen P., Hulthén L., Amann F. W., Bühler F. R. Antihypertensive and renal effects of captopril in relation to renin activity and bradykinin-induced vasodilation. Clin Pharmacol Ther. 1982 Jun;31(6):677–684. doi: 10.1038/clpt.1982.95. [DOI] [PubMed] [Google Scholar]
  5. Mathews K. P., Pan P. M., Gardner N. J., Hugli T. E. Familial carboxypeptidase N deficiency. Ann Intern Med. 1980 Sep;93(3):443–445. doi: 10.7326/0003-4819-93-3-443. [DOI] [PubMed] [Google Scholar]
  6. Regoli D., Barabé J. Pharmacology of bradykinin and related kinins. Pharmacol Rev. 1980 Mar;32(1):1–46. [PubMed] [Google Scholar]
  7. Schapira M., Silver L. D., Scott C. F., Schmaier A. H., Prograis L. J., Jr, Curd J. G., Colman R. W. Prekallikrein activation and high-molecular-weight kininogen consumption in hereditary angioedema. N Engl J Med. 1983 May 5;308(18):1050–1053. doi: 10.1056/NEJM198305053081802. [DOI] [PubMed] [Google Scholar]
  8. Swartz S. L., Williams G. H., Hollenberg N. K., Moore T. J., Dluhy R. G. Converting enzyme inhibition in essential hypertension: the hypotensive response does not reflect only reduced angiotensin II formation. Hypertension. 1979 Mar-Apr;1(2):106–111. doi: 10.1161/01.hyp.1.2.106. [DOI] [PubMed] [Google Scholar]
  9. Wilkin J. K., Hammond J. J., Kirkendall W. M. The captopril-induced eruption. A possible mechanism: cutaneous kinin potentiation. Arch Dermatol. 1980 Aug;116(8):902–905. [PubMed] [Google Scholar]
  10. Wood S. M., Mann R. D., Rawlins M. D. Angio-oedema and urticaria associated with angiotensin converting enzyme inhibitors. Br Med J (Clin Res Ed) 1987 Jan 10;294(6564):91–92. doi: 10.1136/bmj.294.6564.91. [DOI] [PMC free article] [PubMed] [Google Scholar]
  11. Yang H. Y., Erdös E. G., Levin Y. Characterization of a dipeptide hydrolase (kininase II: angiotensin I converting enzyme). J Pharmacol Exp Ther. 1971 Apr;177(1):291–300. [PubMed] [Google Scholar]

Articles from British Journal of Clinical Pharmacology are provided here courtesy of British Pharmacological Society

RESOURCES