Regulation of angiotensin Ⅱ on Gαq/11 protein of vascular smooth muscle cell and its underlying mechanism  

作　　者：XING Dongqi, BAI Hua, ZHAO Yali & WU LilingDepartment of Physiology and Pathophysiology, Peking University Health Science Center, Beijing 100083, China 

出　　处：《Chinese Science Bulletin》2002年第16期1369-1372,共4页

基　　金：This work was supported by the National Natural Science Foundation of China (Grant Nos. 30170379 and 39870356).

摘　　要：To study the regulation of angiotensin Ⅱ (Ang Ⅱ) on Gαq/11 protein of vascular smooth muscle cell (VSMC) and its underlying mechanism, the protein synthesis was detected by [3H]-leucine incorporation. Gαq/11 expression was measured by Western blot in cultured VSMC of rat aorta. The results showed that the level of Gαq/11 was down-regulated after stimulated by Ang Ⅱ for 1-6 h, while it was upregulated significantly by 12-24 h stimulation (P 【 0.01) in VSMC. The [3H]-leucine incorporation of VSMC was increased after 24 h Ang Ⅱ stimulation. The biphase regulation of Ang Ⅱ on Gαq/11 protein was blocked by the Ang Ⅱ type I receptor (AT1) specific antagnist losartan or PLC inhibitor U73122, while PD98059 did not have this effect. These data indicated that Ang Ⅱ contributed to VSMC hypertrophy by regulating the level of Gαq/11, and this effect was mediated mainly through AT1 receptor-PLC signal transduction pathway.To study the regulation of angiotensin II (Ang II) on Gαq/11 protein of vascular smooth muscle cell (VSMC) and its underlying mechanism, the protein synthesis was detected by [3H]-leucine incorporation. Gαq/11 expression was measured by Western blot in cultured VSMC of rat aorta. The results showed that the level of Gαq/11 was down-regulated after stimulated by Ang II for 1-6 h, while it was upregulated significantly by 12-24 h stimulation (P < 0.01) in VSMC. The [3H]-leucine incorporation of VSMC was increased after 24 h Ang II stimulation. The biphase regulation of Ang II on Gαq/11 protein was blocked by the Ang II type I receptor (AT1) specific antagnist losartan or PLC inhibitor U73122, while PD98059 did not have this effect. These data indicated that Ang II contributed to VSMC hypertrophy by regulating the level of Gαq/11, and this effect was mediated mainly through AT1 receptor-PLC signal transduction pathway.

关 键 词：ANGIOTENSIN II vascular smooth muscle cell G PROTEIN HYPERTROPHY signal transduction. 

分 类 号：R363[医药卫生—病理学]