Rapid communicationReduction of infarct size by local angiotensin-converting enzyme inhibition is abolished by a bradykinin antagonist
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Decreased effectiveness of ischemic heart preconditioning in the state of chronic inflammation
2015, Medical HypothesesExtracellular and intracellular proteases in cardiac dysfunction due to ischemia-reperfusion injury
2013, International Journal of CardiologyCitation Excerpt :These products have been shown to be beneficial in reducing arrhythmias and improving contractility [133]. Bradykinin has been reported to reduce infarct size and decrease the duration of reperfusion arrhythmias [134–136]. Observations of increased myocardium protection have been made when endogenous bradykinin deactivation was inhibited causing the release of protective NO and prostaglandin [137–139].
1,5-Benzothiazepine, a versatile pharmacophore: A review
2008, European Journal of Medicinal ChemistryCitation Excerpt :It is highly conserved across all eukaryotes and its expression is essential for biological cells to progress through mitosis. Calmodulin-stimulated protein phosphatase and calmodulin-dependent kinases are the major calmodulin-binding proteins in the brain [94]. Structure of calmoduline protein is shown in Fig. 2.
Pretreatment With Intracoronary Enalaprilat Protects Human Myocardium During Percutaneous Coronary Angioplasty
2007, Journal of the American College of CardiologyCitation Excerpt :If biologically active levels of enalaprilat were still present during balloon inflation, one would have expected the coronary vasodilation to persist. The mechanism whereby enalaprilat induces PC may involve potentiation of bradykinin, which is known to precondition myocardium experimentally (5) and to induce PC in the setting of PTCA (4). Theoretically, it is also possible that the protective effect of enalaprilat may have been triggered by the transient increase in CBF, possibly via endothelial shear-mediated mechanisms.
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