Key Points
- This study aims to explore whether bradykinin affects collagen gene expression through prostaglandin formation in cardiac fibroblasts.
- Bradykinin was applied to cardiac fibroblasts to measure arachidonic acid metabolite release and collagen mRNA levels.
- Dose-dependent effects of bradykinin on 6-keto PGF1alpha release were assessed.
- Indomethacin was used to reverse the effects of bradykinin on collagen gene expression.
- Bradykinin increased [3H]arachidonic acid metabolite release 2.3-fold over control, leading to a 4-fold increase in 6-keto PGF1alpha release at 1 nmol/L concentration.
- Beraprost reduced proalpha1(I) collagen mRNA levels by 35.6% and proalpha1(III) levels by 34.2%.
- Pretreatment with indomethacin reversed bradykinin's effects on collagen type I and III gene expression.
Structured PICO
PPopulationRabbit cardiac fibroblasts
IInterventionBradykinin (with or without indomethacin pretreatment) and Beraprost (PGI2 analogue)
CComparatorControl (untreated cells)
OOutcomeCollagen type I and III gene expression (proalpha1(I) and proalpha1(III) mRNA levels) and arachidonic acid metabolite releasesurrogate
Bradykinin attenuates collagen gene expression in cardiac fibroblasts via prostacyclin production, providing a potential mechanism for the antifibrotic benefits of ACE inhibitors.