Abstract:
BACKGROUND:We tested the hypothesis that long-term administration of the specific angiotensin II subtype 1 (AT1)-receptor blocker BMS-186295 will regress hypertrophy and modify left ventricular angiotensin converting enzyme (ACE) expression in rats with ascending aortic stenosis. METHODS AND RESULTS:Six weeks after surgery, rats with ascending aortic stenosis were randomized to receive either the AT1-receptor blocker BMS-186295 50 mg.kg-1.d-1 (n = 49), amlodipine 2.5 mg.kg-1.d-1 (n = 48) as a positive control for systemic vasodilation, or no drug (n = 48) and compared with sham-operated rats (n = 39). Drug treatment was continued for 15 weeks. Left ventricular ACE mRNA levels were measured by ribonuclease protection assay. The left ventricular/body weight ratio was increased 43% in hearts from rats with untreated left ventricular hypertrophy (LVH) versus control hearts (P < .05). However, there was no difference in either the left ventricular/body weight ratio (2.78 +/- 0.08 versus 2.81 +/- 0.20 mg/g; P = NS) or myocyte cross-sectional area in the AT1-blocker-treated versus untreated LVH hearts. Amlodipine also showed no effect on regression of hypertrophy. In vivo left ventricular systolic pressure was significantly higher in untreated LVH versus sham-operated rats (193 +/- 8 versus 118 +/- 4 mm Hg; P < .05), and there was a similar severe elevation of left ventricular systolic pressure in the AT1-blocker- and amlodipine-treated LVH groups (189 +/- 9 and 188 +/- 16 mm Hg; P = NS versus untreated LVH). In vivo left ventricular end-diastolic pressure was higher in the untreated LVH than in the sham-operated rats (14.8 +/- 2.3 versus 7.0 +/- 0.5 mm Hg; P < .05). Left ventricular end-diastolic pressure was lower in the AT1-blocker-treated (11.0 +/- 1.7 mm Hg) and amlodipine-treated rats (11.5 +/- 1.8 mm Hg) and was similar to left ventricular end-diastolic pressure in the sham-operated rats (P = NS). Left ventricular ACE mRNA levels were elevated in untreated LVH rats but were normalized in both the AT1-blocker-treated rats and amlodipine-treated rats. CONCLUSIONS:Long-term AT1-receptor blockade did not regress LVH in rats with persistent systolic pressure overload due to ascending aortic stenosis. However, both AT1-receptor blockade and amlodipine improved in vivo left ventricular end-diastolic pressure in association with the normalization of left ventricular ACE mRNA levels.
journal_name
Circulationjournal_title
Circulationauthors
Weinberg EO,Lee MA,Weigner M,Lindpaintner K,Bishop SP,Benedict CR,Ho KK,Douglas PS,Chafizadeh E,Lorell BHdoi
10.1161/01.cir.95.6.1592subject
Has Abstractpub_date
1997-03-18 00:00:00pages
1592-600issue
6eissn
0009-7322issn
1524-4539journal_volume
95pub_type
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