Key result
NO synthesis inhibition blunts and ACE inhibition enhances bradykinin-induced coronary vasodilation and blood flow.
Why the study?
Bradykinin causes endothelium-dependent vasodilation, but little is known about the mechanism of bradykinin-induced dilation of coronary arteries in humans in vivo.
Does pretreatment with NO synthesis inhibitor or ACE inhibitor alter bradykinin-induced coronary vasodilation in patients without significant atherosclerotic stenosis?
Does pretreatment with NO synthesis inhibitor or ACE inhibitor alter bradykinin-induced coronary vasodilation in patients without significant atherosclerotic stenosis?
p-value: p=< 0.01
Bradykinin-induced dilation of human coronary arteries is mediated by nitric oxide and enhanced by ACE inhibition.
No takes yet. Share an insight, caveat, or question.
BK coronary dilation is NO-dependent in humans; leaves open whether ACE inhibition meaningfully augments this effect in vivo.
Kuga et al. (1997) studied No significant atherosclerotic stenosis (n=20). Intracoronary bradykinin with L-NMMA or enalaprilat vs. Bradykinin alone was evaluated on Coronary artery diameter and coronary blood flow (p=< 0.01). Bradykinin-induced increases in coronary artery diameter and blood flow were significantly reduced by NO synthesis inhibition (p < 0.01) and increased by ACE inhibition (p < 0.01).
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