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Reduction of infarct size by local angiotensin-converting enzyme inhibition is abolished by a bradykinin antagonist

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    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].

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    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.

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    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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