What is the clinical evidence from this study?

Study design: Other. Intervention: ACE inhibitors (captopril, enalaprilat). Primary outcome: Contractile response to bradykinin and B2 receptor desensitisation.

What does this research mean for the field?

ACE inhibitors potentiate bradykinin responses exclusively through the prevention of its metabolism, without directly preventing kinin B2 receptor desensitisation. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

February 1, 2002Canadian Journal of Physiology and Pharmacology

Studies on the angiotensin-converting enzyme and the kinin B2receptor in the rabbit jugular vein: modulation of contractile response to bradykinin

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Key result

ACE inhibitors potentiate bradykinin exclusively by preventing metabolism but fail to prevent B2 receptor desensitization.

Population

Rabbit jugular vein (rbJV) bioassay system (endothelium-denuded veins)

Comparison

ACE inhibitors (captopril, enalaprilat) vs Tissues not pretreated with ACE inhibitors

Design

Preclinical

Authors

FGFernand GobeilUniversité de Sherbrooke SHStephanie Hallé PBPaul-André BlaisUniversité de Sherbrooke

Discussion

Member takes

Implication

Does not support changes to ACE inhibitor use; leaves open B2 receptor roles in human bradykinin responses.

Structured PICO

Population

Rabbit jugular vein (rbJV) bioassay system (endothelium-denuded veins)

Intervention

ACE inhibitors (captopril, enalaprilat)

Comparator

Tissues not pretreated with ACE inhibitors

Outcome

Contractile response to bradykinin (BK) and BK analogues (pEC50 values)surrogate

ACE inhibitors potentiate bradykinin effects by preventing its metabolism and restoring tissue responsiveness by changing local bradykinin concentrations, rather than by preventing B2 receptor desensitisation.

Cite This Study

Gobeil et al. (2002) studied this question. ACE inhibitors (captopril, enalaprilat) was evaluated on Contractile response to bradykinin and B2 receptor desensitisation. ACE inhibitors potentiate bradykinin exclusively by preventing its metabolism and restore tissue responsiveness by changing bradykinin concentrations, but do not prevent B2 receptor desensitisation.

synapsesocial.com/papers/6aa7801ffb78d07897effdc9 https://doi.org/10.1139/y02-014

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February 1, 2002Canadian Journal of Physiology and Pharmacology

Studies on the angiotensin-converting enzyme and the kinin B2receptor in the rabbit jugular vein: modulation of contractile response to bradykinin

View Full Paper

Ask AI

Bookmark

Key result

ACE inhibitors potentiate bradykinin exclusively by preventing metabolism but fail to prevent B2 receptor desensitization.

Population

Rabbit jugular vein (rbJV) bioassay system (endothelium-denuded veins)

Comparison

ACE inhibitors (captopril, enalaprilat) vs Tissues not pretreated with ACE inhibitors

Design

Preclinical

Authors

FGFernand GobeilUniversité de Sherbrooke SHStephanie Hallé PBPaul-André BlaisUniversité de Sherbrooke

Discussion

Member takes

Implication

Does not support changes to ACE inhibitor use; leaves open B2 receptor roles in human bradykinin responses.

Structured PICO

Population

Rabbit jugular vein (rbJV) bioassay system (endothelium-denuded veins)

Intervention

ACE inhibitors (captopril, enalaprilat)

Comparator

Tissues not pretreated with ACE inhibitors

Outcome

Contractile response to bradykinin (BK) and BK analogues (pEC50 values)surrogate

Cite This Study

synapsesocial.com/papers/6aa7801ffb78d07897effdc9 https://doi.org/10.1139/y02-014

Also Consider

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

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