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AngII activates phospholipase C-\u03b2 (PLC-\u03b2), thereby inducing Ca<jats:sup>2+<\/jats:sup> mobilization as well as the production of reactive oxygen species (ROS). Since contraction is a unique property of contractile VSMCs, signaling cascades related to the proliferation of VSMCs may differ. However, the specific molecular mechanism that controls the contraction or proliferation of VSMCs remains unclear. AngII-induced ROS production, migration, and proliferation were suppressed by inhibiting PLC-\u03b23, inositol trisphosphate (IP<jats:sub>3<\/jats:sub>) receptor, and NOX or by silencing PLC-\u03b23 or NOX1 but not by NOX4. However, pharmacological inhibition or silencing of PLC-\u03b23 or NOX did not affect AngII-induced VSMC contraction. Furthermore, the AngII-dependent constriction of mesenteric arteries isolated from PLC-\u03b23<jats:sup>\u2206SMC<\/jats:sup>, NOX1<jats:sup>\u2212\/\u2212<\/jats:sup>, NOX4<jats:sup>\u2212\/\u2212<\/jats:sup> and normal control mice was similar. AngII-induced VSMC contraction and mesenteric artery constriction were blocked by inhibiting the L-type calcium channel Rho-associated kinase 2 (ROCK2) or myosin light chain kinase (MLCK). The activation of ROCK2 and MLCK was significantly induced in PLC-\u03b23<jats:sup>\u2206SMC<\/jats:sup> mice, whereas the depletion of Ca<jats:sup>2+<\/jats:sup> in the extracellular medium suppressed the AngII-induced activation of ROCK2, MLCK, and vasoconstriction. AngII-induced hypertension was significantly induced in NOX1<jats:sup>\u2212\/\u2212<\/jats:sup> and PLC-\u03b23<jats:sup>\u2206SMC<\/jats:sup> mice, whereas LCCA ligation-induced neointima formation was significantly suppressed in NOX1<jats:sup>\u2212\/\u2212<\/jats:sup> and PLC-\u03b23<jats:sup>\u2206SMC<\/jats:sup> mice. 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