Think about what acute inflammation is designed to achieve: it must deliver more blood and let defensive plasma proteins and cells reach the injured tissue quickly. Both goals depend on the vascular response, which is why that response is treated as the hallmark of the process.
The sequence runs as follows. A momentary narrowing of vessels gives way almost immediately to widening of the arterioles, so flow surges into the capillary bed and the area turns warm and red. At the same time the venular endothelium contracts and pulls apart at junctions, opening gaps through which a protein-rich exudate leaks out, swelling the tissue. The leaked fluid raises local viscosity, slows flow into stasis, and lets neutrophils marginate and emigrate.
Of the choices given, vasoconstriction is only a transient prelude, while stasis and margination are later steps that follow from the permeability change. The single answer that captures the defining vascular event is the combination of dilation and leakiness.
\[\boxed{\text{Vasodilation and increase in permeability}}\]