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

To study the regulation of angiotensin II (Ang II) on Galphaq/11 protein of vascular smooth muscle cell (VSMC) and its underlying mechanism, the protein synthesis was detected by [H-3]-leucine incorporation. Galphaq/11 expression was measured by Western blot in cultured VSMC of rat aorta. The results showed that the level of Galphaq/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 [H-3]-leucine incorporation of VSMC was increased after 24 h Ang II stimulation. The biphase regulation of Ang II on Gaq/11 protein was blocked by the Ang II type I receptor (AT(1)) 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 Galphaq/11, and this effect was mediated mainly through AT, receptor-PLC signal transduction pathway.