Key result
ACE inhibitors potentiated bradykinin-induced endothelium-dependent relaxations in canine coronary arteries by enhancing both nitric oxide release and endothelium-derived hyperpolarizing factor.
Why the study?
Does the addition of ACE inhibitors to bradykinin improve endothelium-dependent relaxations in isolated canine coronary arteries?
Population
Isolated canine coronary arteries
Comparison
ACE inhibitors with bradykinin vs Bradykinin without ACE inhibitors
Design
Preclinical
Authors
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May guide mechanistic research on endothelial function; leaves open translation from canine models to patients.
Does the addition of ACE inhibitors to bradykinin improve endothelium-dependent relaxations in isolated canine coronary arteries?
ACE inhibitors potentiate bradykinin-induced relaxation in canine coronary arteries by enhancing both nitric oxide release and endothelium-derived hyperpolarizing factor.
Mombouli et al. (1992) studied Canine coronary artery physiology. ACE inhibitors (cilazaprilat and perindoprilat) vs. Control (absence of ACE inhibitors) was evaluated on Isometric tension, tissue levels of cGMP, and transmembrane potential. ACE inhibitors potentiated bradykinin-induced endothelium-dependent relaxations in canine coronary arteries by enhancing both nitric oxide release and endothelium-derived hyperpolarizing factor.
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