Either, or both, can cause it.
The key to the correct answer must have been somewhere else in the question stem.
If the patient was recently started on an ACE inhibitor, it's bradykinin. The patient likely has C1 esterase inhibitor deficiency, which (in addition to complement inhibition), is responsible for breaking down kallkrein, which normally produces bradykinin. ACE normally breaks down bradykinin. So you combine a scenario where someone is making excessive amounts of bradykinin and now you've inhibited their ability to metabolize it. Bradykinin causes vasodilation and increased capillary permeability.
Mast cell and basophil degranulation produce histamine. Degranulation can either be IgE-dependent (allergen-induced) or independent (drug-induced). Histamine results in vasodilation and increased capillary permeability.