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Neuronal activity is thought to communicate to arterioles in the brain through astrocytic calcium (Ca²⁺) signaling to cause local vasodilation. Paradoxically, this communication may cause vasoconstriction in some cases. Here, we show that, regardless of the mechanism by which astrocytic endfoot Ca²⁺ was elevated, modest increases in Ca²⁺ induced dilation, whereas larger increases switched dilation to constriction. Large-conductance, Ca²⁺-sensitive potassium channels in astrocytic endfeet mediated a majority of the dilation and the entire vasoconstriction, implicating local extracellular K⁺ as a vasoactive signal for both dilation and constriction. These results provide evidence for a unifying mechanism that explains the nature and apparent duality of the vascular response, showing that the degree and polarity of neurovascular coupling depends on astrocytic endfoot Ca²⁺ and perivascular K⁺.