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July 1, 1997British Journal of PharmacologyOpen Access

ACE inhibitor potentiation of bradykinin‐induced venoconstriction

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Population

Isolated endothelium-denuded segments of the rabbit jugular vein, cultured fibroblasts, and cultured…

Comparison

ACE inhibitors and angiotensin- vs Inhibitors of amino-, carboxy-, metallo- or…

Design

Preclinical

Authors

MHMarkus HeckerUniversity of SaskatchewanABAndree BlaukatUniversity of BernABAgnieszka T. BaraGoethe University Frankfurt

Discussion

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Implication

May warrant caution in extrapolating to human vessels; leaves open whether B2 potentiation contributes to ACE inhibitor effects in vivo.

Key Points

  • This research aims to determine how ACE inhibitors influence bradykinin-induced venoconstriction in isolated blood vessels.
  • Isolated endothelium-denuded segments of rabbit jugular veins were used.
  • The effects of various ACE inhibitors on bradykinin and angiotensin II responses were analyzed.
  • Binding studies for bradykinin to B2 receptors were conducted using radiolabeled compounds.
  • Moexiprilat and ramiprilat increased constrictor response to bradykinin by 3-4 times (p<0.05).
  • Other ACE inhibitors were less effective, with differences in potency noted up to two orders of magnitude.
  • Ramiprilat did not affect bradykinin binding to B2 receptors, indicating potentiation may involve intrinsic activity changes.

Structured PICO

P
Population
Isolated endothelium-denuded segments of the rabbit jugular vein, cultured fibroblasts, and cultured endothelial cells
I
Intervention
ACE inhibitors (moexiprilat, ramiprilat, captopril, enalaprilat, quinaprilat) and angiotensin-(1-7)
C
Comparator
Inhibitors of amino-, carboxy-, metallo- or serine peptidases, synthetic ACE substrate (hippuryl-L-histidyl-L-leucine), or control conditions without ACE inhibitors
O
Outcome
Constrictor response to bradykinin, binding of [3H]-bradykinin to B2 receptors, and cleavage of B2 receptorssurrogate

ACE inhibitors selectively potentiate B2 receptor-mediated vascular effects of bradykinin, likely through an increase in the intrinsic activity of unoccupied B2 receptor molecules rather than by preventing bradykinin degradation or altering receptor affinity.

Cite This Study

Hecker et al. (1997) studied this question.

synapsesocial.com/papers/6a70d73afe4101aa97e056d2https://doi.org/10.1038/sj.bjp.0701281
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1ACE inhibitors are endothelium dependent vasodilators of coronary arteries during submaximal stimulation with bradykinin1993 · 67 citations
  2. 2Endothelium dependent vasomotor responses to endogenous agonists are potentiated following ACE inhibition by a bradykinin dependent mechanism1994 · 56 citations
  3. 3Angiotensin-(1-7) Potentiates the Hypotensive Effect of Bradykinin in Conscious Rats1995 · 160 citations
  4. 4Endothelium-Dependent Vasodilation is Augmented by Angiotensin Converting Enzyme Inhibitors in Healthy Volunteers1992 · 57 citations
  5. 5Endothelium-dependent relaxation by angiotensin-converting enzyme inhibitors in canine femoral arteries1994 · 23 citations