Mechanisms of cardiac hypertrophy in canine volume overload
Departments of Medicine, Physiology, and Cell Biology and Anatomy, Gazes Cardiac Research Institute, and Veterans Affairs Medical Center, Charleston, South Carolina 29403 This study tested whether the modest hypertrophy that develops in dogs in response to mitral regurgitation is due to a relatively...
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Published in | American journal of physiology. Heart and circulatory physiology Vol. 275; no. 1; pp. H65 - H74 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
01.07.1998
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Subjects | |
Online Access | Get full text |
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Summary: | Departments of Medicine, Physiology, and Cell Biology and Anatomy,
Gazes Cardiac Research Institute, and Veterans Affairs Medical Center,
Charleston, South Carolina 29403
This study tested whether the modest hypertrophy
that develops in dogs in response to mitral regurgitation is due to a
relatively small change in the rate of protein synthesis or,
alternatively, is due to a decreased rate of protein degradation. After
3 mo of severe experimental mitral regurgitation, the left ventricular (LV) mass-to-body weight ratio increased by 23% compared with baseline
values. This increase in LV mass occurred with a small, but not
statistically significant, increase in the fractional rate of myosin
heavy chain (MHC) synthesis
(K s ), as measured using continuous infusion with
[ 3 H]leucine in dogs at
2 wk, 4 wk, and 3 mo after creation of severe mitral regurgitation.
Translational efficiency was unaffected by mitral regurgitation as
measured by the distribution of MHC mRNA in polysome gradients.
Furthermore, there was no detectable increase in translational capacity
as measured by either total RNA content or the rate of ribosome
formation. These data indicate that translational mechanisms that
accelerate the rate of cardiac protein synthesis are not responsive to
the stimulus of mitral regurgitation. Most of the growth after mitral
regurgitation was accounted for by a decrease in the fractional rate of
protein degradation, calculated by subtracting fractional rates of
protein accumulation at each time point from the corresponding
K s values. We conclude that
1 ) volume overload produced by
severe mitral regurgitation does not trigger substantial increases in
the rate of protein synthesis and 2 )
the modest increase in LV mass results primarily from a decrease in the
rate of protein degradation.
heart; myosin; mitral regurgitation; protein synthesis |
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ISSN: | 0363-6135 0002-9513 1522-1539 |
DOI: | 10.1152/ajpheart.1998.275.1.h65 |