@entity1809 receptor blockade increases cardiac @entity1812 via neutral endopeptidase after induction of @entity583 in XXXX .

@entity8123 @entity9383 @entity63 @entity1809 @entity1563 @entity1808 @entity7056 @entity1812 @entity35 @entity583
ACE inhibition protects the heart against @entity63 by reducing @entity1808 and promoting @entity1812 (BK) accumulation. Since neutral endopeptidase ( @entity8123 ) metabolizes BK, we determined its activity after induction of @entity583 ( @entity583 ) and examined whether it is influenced by treatment with an ACE inhibitor or @entity1809 receptor blocker. @entity35 were studied 6 days and 3 wk after @entity1563 . Starting 48 h after @entity583 induction, additional animals were treated with the ACE inhibitor @entity9383 (2 mg x kg(-1) x day-1) or the @entity1809 blocker @entity7056 (50 mg x kg(-1) x day-1). Animals were hemodynamically characterized. Finally, @entity8123 -specific activity and BK concentrations were detected in homogenates of heart compartments. @entity9383 and @entity7056 treatment improved left ventricular function 6 days and 3 wk after @entity583 induction, and @entity8123 activity was elevated only in the infarcted area of untreated compared with sham-operated @entity35 . After 6 days, @entity7056 reversed this increase by 80% and @entity9383 by 35%. @entity9383 had no effect after 3 wk, whereas @entity7056 almost completely blocked the increased @entity8123 activity in the infarcted area and concomitantly induced a further rise in the BK concentrations. These results indicate mechanisms of @entity8123 regulation influenced by the @entity1809 receptor. Our data suggest that @entity8123 is more decisive than ACE in mediating BK degradation and may indicate BK involvement in the cardioprotective effects of @entity1809 antagonists.
