What question did this study set out to answer?

To determine whether thin-filament contractile proteins undergo an adult-to-fetal isoform transition during cardiac hypertrophy and its regression following enalapril therapy in spontaneously hypertensive rats.

December 1, 1990HypertensionOpen Access

Regression of cardiac hypertrophy in spontaneously hypertensive rats by enalapril and the expression of contractile proteins.

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Why the study?

Does enalapril reduce cardiac hypertrophy and alter contractile protein expression in spontaneously hypertensive rats?

Population

12-week-old spontaneously hypertensive rats (SHR)

Comparison

Enalapril treatment for 2, 5, 8, and 9 weeks… vs Weight- and age-matched control SHR without drug…

Design

Preclinical

Follow-up

Up to 18 weeks (9 weeks treatment + 9 weeks withdrawal)

Authors

TCTimothy ChildsKingston Health Sciences Centre MAMichael A. AdamsLawrence Berkeley National Laboratory AMAlan S. MakQueen's University

Discussion

Member takes

Implication

Enalapril-linked LVH regression and myosin shift in SHR models; leaves open translation to human hypertensive heart disease.

Key Points

To determine whether thin-filament contractile proteins undergo an adult-to-fetal isoform transition during cardiac hypertrophy and its regression following enalapril therapy in spontaneously hypertensive rats.
Treated 12-week-old spontaneously hypertensive rats (SHR) with the angiotensin-converting enzyme inhibitor enalapril for 2, 5, 8, and 9 weeks, followed by a 9-week drug withdrawal period.
Compared treated animals to age- and weight-matched untreated control SHR, measuring mean arterial blood pressure, left ventricular weight-to-body weight ratio, and contractile protein isoform expressions.
Nine weeks of enalapril reduced mean arterial blood pressure (from 166 ± 11 to 89 ± 5 mm Hg) and regressed left ventricular weight-to-body weight ratio (from 2.53 ± 0.14 to 1.96 ± 0.05 g/kg) to normal levels.
Fetal V3 myosin heavy chain decreased from 35 ± 3% to 13 ± 1% with enalapril, significantly correlating with left ventricular mass regression (r = 0.697, p < 0.001).
Only adult isoforms of tropomyosin and troponin T were detected in SHR with or without enalapril, and tropomyosin phosphorylation remained unchanged despite changes in ventricular mass.

Structured PICO

Does enalapril reduce cardiac hypertrophy and alter contractile protein expression in spontaneously hypertensive rats?

Population

12-week-old spontaneously hypertensive rats (SHR)

Intervention

Enalapril treatment for 2, 5, 8, and 9 weeks followed by withdrawal of treatment for 9 weeks

Comparator

Weight- and age-matched control SHR without drug treatment

Outcome

Expression of isoforms of myosin, tropomyosin, and troponin T in the left ventricle, and phosphorylation of tropomyosinsurrogate

Enalapril induces regression of left ventricular hypertrophy and reduces fetal V3 myosin expression in spontaneously hypertensive rats, but does not alter tropomyosin or troponin T isoforms.

Cite This Study

Childs et al. (1990) studied this question.

synapsesocial.com/papers/6a779180576efb0ddaf7733f https://doi.org/10.1161/01.hyp.16.6.662

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Regression of cardiac hypertrophy in spontaneously hypertensive rats by enalapril and the expression of contractile proteins.

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Regression of cardiac hypertrophy in spontaneously hypertensive rats by enalapril and the expression of contractile proteins.

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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