Regulation of angiotensinⅡon Gαq/11 protein of vascular smooth muscle cell and its underlying mechanism

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 downregulated after stimulated by AngⅡ 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.