Figure 1.

Back-propagation of vasodilation through astrocyte vascular endfeet. As outlined in Witthoft et al. (11), large-activity-induced potassium increases will result in astrocyte depolarization and siphoning of excess potassium to the gliovascular interface, where it activates inwardly rectifying potassium channels on arteriole smooth muscle, resulting in hyperpolarization and relaxation/dilation. This dilation results in stretch of glial foot processes and opening of TRPV4 channels, allowing calcium in to activate BK channels. This will further flood the perivascular space with potassium, enlarging and expanding the dilatory response. As the dilation expands, the stretch will activate TRPV4 channels on the adjacent nonstimulated astrocyte process, initiating the same processes leading to further dilation. This cascade can jump from foot process to foot process being regenerated with each jump, much like saltatory jumping of the action potential down myelinated fibers. In this way, local dilatory signals can rapidly propagate back up the vascular tree to dilate the larger supply arteries.