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1 Cardiovascular Division, Department of Internal Medicine, Institute of Clinical Medicine, 2 Gene Experiment Center, Institute of Applied Biochemistry, and 3 Institute of Health and Sport Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-0006, Japan
Pressure overload,
such as hypertension, to the heart causes pathological cardiac
hypertrophy, whereas chronic exercise causes physiological cardiac
hypertrophy, which is defined as athletic heart. There are differences
in cardiac properties between these two types of hypertrophy. We
investigated whether mRNA expression of various cardiovascular
regulating factors differs in rat hearts that are physiologically and
pathologically hypertrophied, because we hypothesized that these two
types of cardiac hypertrophy induce different molecular phenotypes. We
used the spontaneously hypertensive rat (SHR group; 19 wk old) as a
model of pathological hypertrophy and swim-trained rats (trained group;
19 wk old, swim training for 15 wk) as a model of physiological
hypertrophy. We also used sedentary Wistar-Kyoto rats as the control
group (19 wk old). Left ventricular mass index for body weight was
significantly higher in SHR and trained groups than in the control
group. Expression of brain natriuretic peptide, angiotensin-converting
enzyme, and endothelin-1 mRNA in the heart was significantly higher in
the SHR group than in control and trained groups. Expression of
adrenomedullin mRNA in the heart was significantly lower in the trained
group than in control and SHR groups. Expression of
1-adrenergic receptor mRNA in the heart was
significantly higher in SHR and trained groups than in the control
group. Expression of 1-adrenergic receptor kinase mRNA,
which inhibits 1-adrenergic receptor activity, in the
heart was markedly higher in the SHR group than in control and trained
groups. We demonstrated for the first time that the manner of mRNA
expression of various cardiovascular regulating factors in the heart
differs between physiological and pathological cardiac hypertrophy.
cardiovascular regulating factor; athletic heart; spontaneously hypertensive rat; swim training; hypertension
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