| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1998: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 1997: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Research Abstract |
Mechanical stimuli and many humoral factors, including angiotensin II, are known to be involved in the formation and development of pathological cardiac hypertrophy. On the other hand, there are very few reports with respect to physiological and molecular characteristics of exercise-induced cardiac hypertrophy as well as the mechanisms of the formation and development of this type of hypertrophy. To clarify whether essential differences are present between exercise- and hypertension-induced hypertrophies, we have compared hemodynamics and expression levels of mRNAs that encode molecules associated with cardiac functions between these two forms of hypertrophied rat hearts.
We have obtained the following results.
1. An antagonist for angiotensin II type 1 receptor, which plays a critical role in the formation of hypertension-induced cardiac hypertrophy, did not inhibit cardiac hypertrophy induced by swimming exercise.
2. The mRNA level of sarcoplasmic reticulum Ca^<2+>-ATPase, which regulates cardiac relaxation via intracellular Ca^<2+> uptake in sarcoplasmic reticulum, was higher in left ventricular myocardium in the exercise rats than that in the hypertension rats.
3. The mRNA level of the apoptosis-promoting factor bax was increased in the exercise group, whereas that of the apoptosis-inhibitory factor bcl-2 was increased in both groups of rats.
4. Short-term exercise induced a transient decrease in cardiac MAP kinase (ERK) activity, although activation of ERK is thought to be an key event for the formation of pathological cardiac hypertrophy.
These results strongly demonstrate that the exercise-induced cardiac hypertrophy is formed in a mechanism essentially different from the pathological cardiac hypertrophy, and that their molecular phenotypes and physiological features are also distinct from each other.
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