Antihypertensive effect of gomisin A from Schisandra chinensis on angiotensin II-induced hypertension via preservation of nitric oxide bioavailability

被引:35
作者
Park, Ji Young [1 ,2 ]
Yun, Jung Wook [1 ,2 ]
Choi, Young Whan [3 ]
Bae, Jin Ung [1 ,2 ]
Seo, Kyo Won [1 ,2 ]
Lee, Seung Jin [1 ,2 ]
Park, So Youn [1 ,2 ]
Hong, Ki Whan [1 ,2 ]
Kim, Chi Dae [1 ,2 ]
机构
[1] Pusan Natl Univ, Sch Med, Dept Pharmacol, Yangsan 626870, Gyeongnam, South Korea
[2] Pusan Natl Univ, MRC Ischem Tissue Regenerat, Yangsan 626870, Gyeongnam, South Korea
[3] Pusan Natl Univ, Coll Nat Resources & Life Sci, Yangsan 626870, Gyeongnam, South Korea
关键词
angiotensin II; gomisin A; nitric oxide; ROS; ENDOTHELIAL DYSFUNCTION; NADPH OXIDASE; NAD(P)H OXIDASE; SYNTHASE; ANTIOXIDANT; LIGNANS; CELLS; ENOS;
D O I
10.1038/hr.2012.50
中图分类号
R6 [外科学];
学科分类号
1002 ; 100210 ;
摘要
Gomisin A (GA) is a small molecular weight lignan present in Schisandra chinensis, and has been demonstrated to have vasodilatory activity. In the present study, we investigated the effect of GA on blood pressure (BP) in angiotensin II (Ang II)-induced hypertensive mice. C57/BL6 mice infused subcutaneously with Ang II (1 and 2 mu g kg(-1) per min for 2 weeks) showed an increase in BP with a decrease in nitric oxide (NO) metabolites in plasma, and a negative correlation between these two parameters was demonstrated. In the thoracic aorta from Ang II-induced hypertensive mice, a decrease in vascular NO that was accompanied by a diminution of phosphorylated endothelial nitric oxide synthase (eNOS), as well as by increased reactive oxygen species (ROS) production, was demonstrated. These alterations in BP, eNOS phosphorylation and ROS production in the vasculature of Ang II-treated mice were markedly and dose-dependently reversed by simultaneous administration of GA (2 and 10 mu g kg(-1) per min). In addition, Ang II-induced ROS production in cultured vascular cells such as endothelial cells and vascular smooth muscle cells was markedly attenuated by GA. These results suggested that GA attenuated the increase in BP via preservation of vascular NO bioavailability not only by inhibiting ROS production but also by preventing the impairment of eNOS function in the vasculature of Ang II-induced hypertensive mice. Hypertension Research (2012) 35, 928-934; doi:10.1038/hr.2012.50; published online 26 April 2012
引用
收藏
页码:928 / 934
页数:7
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