Comparative study on hypertension-induced and exercise-induced cardiac hypertrophy with respect to their formation and molecular characteristics.

机械刺激和许多体液因子，包括血管紧张素II，被认为参与了病理性心肌肥厚的形成和发展。另一方面，有关运动性心肌肥厚的生理和分子特征以及这种肥厚的形成和发展机制的报道很少。为了阐明运动性和高血压诱导的肥厚之间是否存在本质差异，我们比较了这两种形式的肥厚大鼠心脏的血流动力学和编码与心功能相关分子的mRNAs的表达水平。我们获得了以下结果。结论1.血管紧张素II 1型受体拮抗剂在高血压心肌肥厚的形成中起关键作用，但不能抑制游泳运动诱导的心肌肥厚。运动组大鼠左室心肌肌浆网Ca~(2+)&lt；2+&gt；-ATPase的mRNA水平高于高血压组，肌浆网通过肌浆网摄取Ca~(2+)&gt；-ATPase调节心肌松弛。运动组大鼠促凋亡因子bax的mRNA水平升高，而凋亡抑制因子bc1-2的mRNA水平升高。尽管ERK的激活被认为是病理性心肌肥厚形成的关键事件，但短期运动可引起心脏MAPK活性的一过性下降。这些结果有力地表明，运动性心肌肥厚的形成机制与病理性心肌肥厚有着本质的不同，它们的分子表型和生理特征也是不同的。

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.