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Role of inducible nitric oxide synthase in the vascular smooth muscle cells cycle arrest induced by 17#beta#-estradiol

Yang Dan, Fu Xiaodong, Li Yongyong, Tan Zhi, Wang Tinghuai, Pan Jingyun

Department of Physiology,Sun Yat-sen University,Zhongshan Medical College.Guangzhou 510089,Guangdong

Abstract

30min and 12h. These effects were significantly inhibited by estrogen receptor (ER) antagonist Tamoxifen (0.1 #mu#mol/L) and NOS inhibitor L-NAME (1 #mu#mol/L). E_(2) increased iNOS protein expression of VSMCs in a dose-dependent manner. The effect of E_(2) on iNOS protein expression of VSMCs started at 3 h, distinctly increased at 12 h and then decreased. Tamoxifen significantly inhibited the E_(2)-induced iNOS protein expression of VSMCs. ET-1 increased cell percentage of S phase and G_(2)+S/G_(1). This effect was inhibited by E_(2). L-NAME significantly attenuated the inhibitory effect of E_(2) on cell cycle of VSMCs. The results suggest that E_(2) induced G_(1) arrest of VSMCs, which was associated with an increase in iNOS activity and protein expression of VSMCs. These effects were at least mediated by estrogen receptor partly.

Key words: Vascular smooth muscle;Estrogen;Nnitric oxide;nitric oxide synthase;Cell cycle

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Citing This Article：

Yang Dan, Fu Xiaodong, Li Yongyong, Tan Zhi, Wang Tinghuai, Pan Jingyun. Role of inducible nitric oxide synthase in the vascular smooth muscle cells cycle arrest induced by 17#beta#-estradiol. Acta Physiol Sin 2003; 55 (6): (in Chinese with English abstract).