The link between myocardial contraction and relaxation: the effects of XXXX antagonists.

@entity268 @entity1855 @entity141 @entity2701 @entity3044 @entity460 @entity594 @entity35
In isolated @entity35 hearts perfused at constant coronary flow and heart rate the amount of shortening in their major axis (L), the developed @entity2701 ( @entity2701 ) and their time derivatives (L and @entity2701 ) were measured after different interventions. Relative changes of maximal velocities of contraction (+L, + @entity2701 ) and relaxation (-L, - @entity2701 ) were assessed by the ratio between both velocities (+L/-L, + @entity2701 /- @entity2701 ). After the interventions, @entity268 intracellular levels and @entity268 dependent protein kinase activity were measured. The negative inotropic effect of @entity1855 (10(-7) M) and @entity594 (5 X 10(-7) M) was accompanied by a relatively greater decrease in maximal velocity of relaxation. Consequently the ratio +L/-L increased. @entity1855 increased +L/-L from 1.27 +/- 0.07 to 1.57 +/- 0.08 (P less than 0.001). @entity594 increased +L/-L from 1.25 +/- 0.05 to 1.77 +/- 0.12 (P less than 0.001). Whereas @entity594 increased intracellular @entity268 levels from 0.403 +/- 0.036 pmol/mg wet weight to 0.534 +/- 0.047 (P less than 0.05), @entity1855 did not alter them. Neither @entity1855 nor @entity594 affected @entity268 protein kinase activity. Increasing @entity141 in the perfusate did not change the ratio +L/-L. A decrease in extracellular @entity141 , on the other hand, produced a greater decrease in -L than in +L, so that the ratio +L/-L increased from 1.27 +/- 0.05 to 1.49 +/- 0.10 (P less than 0.05). No changes were detected in @entity268 levels or its protein kinase activity. Similar results were obtained when + @entity2701 /- @entity2701 was analyzed. To offset the negative inotropic effect caused by @entity460 antagonists, either increased extracellular @entity141 or @entity3044 can be used.(ABSTRACT TRUNCATED AT 250 WORDS)
