Angiotensin II (Ang II) is a pleiotropic hormone that influences the function of many cell types and regulates many organ systems. In the cardiovascular system, it is a potent vasoconstrictor that increases peripheral vascular resistance and elevates arterial pressure. It also promotes inflammation, hypertrophy, and fibrosis, which are important in vascular remodeling in cardiovascular diseases. The diverse actions of Ang II are mediated via AT1 and AT2 receptors, which couple to many signaling molecules, including small G proteins, phospholipases, mitogen-activated protein (MAP) kinases, phosphatases, tyrosine kinases, NADPH oxidase, and transcription factors. In general, acute Ang II stimulation induces vasoconstriction through changes in the intracellular free calcium concentration [Ca2+]i, whereas long-term stimulation leads to cell proliferation and proinflammatory responses. This review focuses on signaling processes of vasoconstriction and highlights some new mechanisms regulating the contractile machinery in controlling vasomotor tone by Ang II, including RhoA/Rho kinase, transient receptor potential (TRP) channels, reactive oxygen species, and arachidonic acid metabolites.