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Articles in PresS, published online ahead of print January 4, 2002
J Appl Physiol, 10.1152/jap.01192.2001
Submitted on December 3, 2001
Accepted on December 31, 2001
1 Dept. of Physiology, Fudan University, Shanghai, Shanghai, China
* To whom correspondence should be addressed. E-mail: yczhu{at}shmu.edu.cn.
We used cultured neonatal rat cardiac myocytes to test the hypothesis that all-trans retinoic acid (atRA) may act to modulate Angiotensin II (Ang II) actions in inducing myocyte hypertrophy. Our observations were as follows. 1) atRA (10-7~10-5M ) inhibited Ang II-induced hyperplasia of fibroblasts in a dose-dependent manner; 2)Treatment of atRA attenuated the Ang II induced increase of total cell protein content; 3) Treated with Ang II (10-7M) for 5 days, the cultured neonatal rat cardiac myocytes demonstrated an apparent accumulation of sarcomeric fibers proteins and Golgi's complex, as well as reorganization of the sarcomeric unit within individual myocyte. atRA (10-6M) treatment reduced the accumulation of contractile proteins and Golgi's complex without affecting the Ang II-induced reorganization of the sarcomeric unit; 4) atRA attenuated the Ang II-induced increase of intracellular Ca2+. Our results show that atRA inhibits some effects of Ang II on neonatal rat cardiac myocytes, and it suggests that atRA may be a therapeutic candidate for the prevention and therapy of cardiac hypertrophy and remodeling.
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