Inhibition of the @entity2814 ( @entity2814 ) in developing left ventricular (LV) @entity1184 has been demonstrated to have inhibitory effects on myocardial growth. An important mechanism of action of @entity2814 inhibition is modulation of myocardial AT1 Ang II-receptor activity. However, whether and to what extent AT1 Ang II-receptor blockade may influence LV and myocyte function during the @entity1184 remains unclear. Accordingly, our project examined the relation between changes in LV and myocyte function during the LV @entity1184 that occurs after recovery from long-term rapid pacing. @entity235 were randomly assigned to the following treatment groups: (a) Pace and Recovery, long-term rapid pacing (4 weeks; 216 +/- 2 beats/min) followed by a 4-week recovery period (n = 6); (b) Recovery/AT1 Block, concomitant AT1 Ang II-receptor blockade [ @entity7056 ( @entity7056 ; @entity7056 ) 30 mg/kg b.i.d.] administered during the 4-week recovery period (n = 5); and (c) Control, sham controls (n = 6). There was no difference in mean arterial pressure in any of the three groups. With pacing and recovery, LV end-diastolic volume and mass were increased by >50% from control values. The significant LV remodeling that occurred with recovery from long-term rapid pacing was associated with a decline in LV ejection fraction (59 +/- 3% vs. 68 +/- 4%) and myocyte velocity of shortening (43 +/- 3 microm/s vs. 63 +/- 3 microm/s) when compared with controls (p < 0.05). With recovery from long-term rapid pacing, LV myocyte length (176 +/- 6 microm vs. 150 +/- 1 microm) and cross-sectional area were increased (292 +/- 7 microm2 vs. 227 +/- 6 microm2) compared with controls (p < 0.05). With AT1 Ang II block during recovery from rapid pacing, LV end-diastolic volume was similar to untreated recovery values, but LV mass was normalized. LV ejection fraction was not different from control values with AT1 Ang II-receptor block. Steady-state myocyte velocity of shortening with AT1 Ang II block was similar to control values (55 +/- 5 microm/s), but percentage shortening remained reduced from control (3.55 +/- 0.37% vs. 4.71 +/- 0.12%, respectively, p < 0.05) and was similar to untreated recovery (3.59 +/- 0.23%). With AT1 Ang II block, myocyte length was similar to untreated recovery values, but cross-sectional area was reduced (260 +/- 5 microm2, p < 0.05). Thus AT1 Ang II-receptor blockade instituted in this model of developing @entity4346 , significantly reduced LV mass but did not reduce the degree of @entity5988 . The cellular basis for these effects of AT1 Ang II-receptor blockade included persistent abnormalities in LV myocyte geometry. AT1 Ang II-receptor blockade improved certain indices of myocyte contractile function from untreated @entity1184 values. These findings suggest that in this pacing-recovery model, the development of @entity4346 and myocyte contractile dysfunction may be caused, at least in part, by AT1 Ang II-receptor activation.

Angiotensin II subtype-1 receptor blockade during the development of @entity4346 in XXXX : effects on ventricular and myocyte function.

@entity5988 :: ('MESH:C565277', 'Disease') :: ['LV dilation'] @entity1184 :: ('MESH:D006984', 'Disease') :: ['hypertrophy', 'hypertrophic process'] @entity2814 :: ('610668(Tax:9615)', 'Gene') :: ['ACE', 'angiotensin-converting enzyme'] @entity235 :: ('9615', 'Species') :: ['Dogs'] @entity7056 :: ('MESH:C081309', 'Chemical') :: ['irbesartan', 'SR 47436', 'BMS-186295'] @entity4346 :: ('MESH:D017379', 'Disease') :: ['LV hypertrophy']
@entity235 :: (9615,Species) :: ['dogs']
