Neurovascular coupling (NVC) represents the mechanisms whereby an increase in neuronal activity (NA) may lead to local vasodilation and increase in regional cerebral blood flow (CBF). It has long been thought that neurons and astrocytes generate the vasoactive mediators regulating local changes in CBF, whereas cerebrovascular endothelial cells are not able to directly sense NA. Unexpectedly, recent evidence demonstrated that brain microvascular endothelial cells may sense NA through inward-rectifier K⁺ (K_ir2.1) channels and may detect synaptic activity via N-methyl-d-aspartate (NMDA) receptors (NMDARs). In the present perspective, therefore, we discuss the hypothesis that endothelial K_ir2.1 channels and NMDARs play a key role in NVC and in CBF regulation, which is crucial to unravel the cellular and molecular underpinnings of blood oxygen level-dependent signals.

神经血管耦合 (NVC) 代表了神经元活动 (NA) 增加可能导致局部血管舒张和局部脑血流量 (CBF) 增加的机制。长期以来，人们一直认为神经元和星形胶质细胞产生调节 CBF 局部变化的血管活性介质，而脑血管内皮细胞不能直接感知 NA。出乎意料的是，最近的证据表明，脑微血管内皮细胞可通过向内整流K感测NA ⁺（K _IR 2.1）信道，并且可以经由N-甲基检测突触活动d天冬氨酸（NMDA）受体（NMDA受体）。因此，从目前的角度来看，我们讨论的假设是内皮细胞 K _ir2.1 通道和 NMDAR 在 NVC 和 CBF 调节中起着关键作用，这对于解开血氧水平依赖性信号的细胞和分子基础至关重要。