Hypoxic culture of brain endothelial cells (BEC) caused membrane hyperpolarization.
This hyperpolarization was due to the increased expression of Kir2.1 channels.
Hypoxia enhanced store-operated Ca2+ (SOC) entry via Kir2.1 up-regulation.
Expression levels of putative SOC channels were not affected by hypoxia.
Kir2.1 up-regulation is responsible for hypoxia-enhanced BEC proliferation.