Effect of Captopril on the bradykinin‐induced release of prostacyclin from guinea‐pig lungs and bovine aortic endothelial cells
Key result
Captopril enhances bradykinin-stimulated prostacyclin in guinea-pig lungs but not in bovine aortic endothelial cells.
Why the study?
The role of angiotensin converting enzyme activation in the release of prostacyclin and EDRF from guinea-pig lungs and bovine aortic endothelial cells was unclear.
Population
Guinea-pig isolated lungs and bovine aortic endothelial cells
Comparison
Captopril (10 microM) vs no captopril
Design
Preclinical experimental study
Authors
Discussion
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Member takes
Implication
Cautions against extrapolating ACE effects on endothelial mediators across species or tissues; leaves open bradykinin-independent mechanisms in vivo.
Structured PICO
P
Population
Guinea-pig isolated lungs perfused with Krebs solution and bovine aortic endothelial cells grown on microcarrier beads
I
Intervention
Captopril (10 microM)
O
Outcome
Bradykinin-induced release of prostacyclin and endothelium-derived relaxing factor (EDRF)surrogate
Activation of angiotensin converting enzyme is not involved in the release of prostacyclin or EDRF from bovine aortic endothelial cells.
Cite This Study
Nucci et al. (1988) studied this question. Captopril was evaluated on Bradykinin-induced release of prostacyclin and EDRF. Captopril enhanced bradykinin-stimulated prostacyclin output in guinea-pig lungs but did not affect prostacyclin or EDRF release in bovine aortic endothelial cells.