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Effects of converting enzyme inhibition on endothelial bradykinin metabolism and endothelium-dependent vascular relaxation.

C. Bossaller, Wolfgang Auch–Schwelk, Michael Gräfe, Klaus Gräf, C. Baumgarten, Eckart Fleck

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Abstract

The effects of ACE-inhibitors on bradykinin metabolism and bradykinin-induced endothelium-dependent relaxation were studied in isolated coronary arteries and endothelial cells in culture. The results suggest that ACE-inhibitors affect coronary vascular tone by at least two endothelium-dependent and bradykinin-mediated mechanisms: First, ACE-inhibitors decrease endothelial bradykinin degredation which is accompanied by an augmented bradykinin mediated endothelium-dependent relaxation. Second, ACE-inhibitors evoke endothelium-dependent relaxations in coronary arteries stimulated with threshold concentrations of bradykinin, which cannot be attributed to an inhibition of bradykinin degradation. The effect appears to represent a new mechanism which may be based on an interaction of the bradykinin receptor and the angiotensin converting enzyme on the cellular level.

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The effects of ACE-inhibitors on bradykinin metabolism and bradykinin-induced endothelium-dependent relaxation were studied in isolated coronary arteries and endothelial cells in culture. The results suggest that ACE-inhibitors affect coronary vascular tone by at least two endothelium-dependent and bradykinin-mediated mechanisms: First, ACE-inhibitors decrease endothelial bradykinin degredation which is accompanied by an augmented bradykinin mediated endothelium-dependent relaxation. Second, ACE-inhibitors evoke endothelium-dependent relaxations in coronary arteries stimulated with threshold concentrations of bradykinin, which cannot be attributed to an inhibition of bradykinin degradation. The effect appears to represent a new mechanism which may be based on an interaction of the bradykinin receptor and the angiotensin converting enzyme on the cellular level.

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Available abstract

The effects of ACE-inhibitors on bradykinin metabolism and bradykinin-induced endothelium-dependent relaxation were studied in isolated coronary arteries and endothelial cells in culture. The results suggest that ACE-inhibitors affect coronary vascular tone by at least two endothelium-dependent and bradykinin-mediated mechanisms: First, ACE-inhibitors decrease endothelial bradykinin degredation which is accompanied by an augmented bradykinin mediated endothelium-dependent relaxation. Second, ACE-inhibitors evoke endothelium-dependent relaxations in coronary arteries stimulated with threshold concentrations of bradykinin, which cannot be attributed to an inhibition of bradykinin degradation. The effect appears to represent a new mechanism which may be based on an interaction of the bradykinin receptor and the angiotensin converting enzyme on the cellular level.

Key concepts: Bradykinin, Endothelium, Angiotensin-converting enzyme, Internal medicine, Chemistry, Bradykinin receptor, Endocrinology, Enzyme

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Effects of converting enzyme inhibition on endothelial bradykinin metabolism and endothelium-dependent vascular relaxation. — Research Paper | ScholarLens