The phosphoinositide, phosphatidylinositol 4,5-bisphosphate (PIP₂), has long been established as a major contributor to intracellular signaling, primarily by virtue of its role as a substrate for phospholipase C (PLC). Signaling by G_q-protein–coupled receptors triggers PLC-mediated hydrolysis of PIP₂ into inositol 1,4,5-trisphosphate and diacylglycerol, which are well known to modulate vascular ion channel activity. Often overlooked, however, is the role PIP₂ itself plays in this regulation. Although numerous reports have demonstrated that PIP₂ is critical for ion channel regulation, how it impacts vascular function has received scant attention. In this review, we focus on PIP₂ as a regulator of ion channels in smooth muscle cells and endothelial cells—the two major classes of vascular cells. We further address the concerted effects of such regulation on vascular function and blood flow control. We close with a consideration of current knowledge regarding disruption of PIP₂ regulation of vascular ion channels in disease.

长期以来，磷酸肌醇、磷脂酰肌醇 4,5-二磷酸 (PIP ₂ ) 一直被确定为细胞内信号传导的主要贡献者，主要是由于其作为磷脂酶 C (PLC) 底物的作用。G _q蛋白偶联受体的信号触发 PLC 介导的 PIP ₂水解成肌醇 1,4,5-三磷酸和甘油二酯，众所周知，它们可调节血管离子通道活性。然而，经常被忽视的是 PIP ₂本身在该法规中所扮演的角色。尽管大量报告表明 PIP ₂对离子通道调节至关重要，但它如何影响血管功能却很少受到关注。在本次审查中，我们重点关注 PIP ₂作为平滑肌细胞和内皮细胞（血管细胞的两大类）中离子通道的调节剂。我们进一步讨论了这种调节对血管功能和血流控制的协同作用。最后，我们考虑了有关破坏疾病中血管离子通道的 PIP ₂调节的当前知识。