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Significance Capillaries, the smallest blood vessels, mediate the on-demand delivery of oxygen and nutrients required to support the function of active cells throughout the brain. But how blood flow is directed to cells in active brain regions to satisfy their energy needs is poorly understood. We demonstrate that the plasma membrane phospholipid, PIP2 , is fundamental to sustaining the activity of inwardly rectifying potassium channels—the molecular feature that allows capillary endothelial cells to sense ongoing neuronal activity and trigger an increase in local blood flow. We further show that chemical factors released in the brain, including those associated with neuronal activity, cause changes in the levels of PIP2 , thereby altering endothelial potassium channel signaling and controlling cerebral blood flow.

Endothelial GqPCR activity controls capillary electrical signaling and brain blood flow through PIP 2 depletion

Endothelial GqPCR activity controls capillary electrical signaling and brain blood flow through PIP ₂ depletion