Does the release of potassium from astrocyte endfeet regulate cerebral blood flow?

Abstract

Local increases in neuronal activity within the brain lead to dilation of blood vessels and to increased regional cerebral blood flow. Increases in extracellular potassium concentration are known to dilate cerebral arterioles. Recent studies have suggested that the potassium released by active neurons is transported through astrocytic glial cells and released from their endfeet onto blood vessels. The results of computer simulations of potassium dynamics in the brain indicate that the release of potassium from astrocyte endfeet raises perivascular potassium concentration much more rapidly and to higher levels than does diffusion of potassium through extracellular space, particularly when the site of a potassium increase is some distance from the vessel wall. On the basis of this finding, it is proposed that the release of potassium from astrocyte endfeet plays an important role in regulating regional cerebral blood flow in response to changes in neuronal activity.

Fig. 1

Simulation of the [K⁺] buildup at the external wall of an arteriole after an imposed, instantaneous rise in [K⁺]_o from 3 to 10 mM within the brain. Transport of K⁺ from the region of [K⁺]_o increase to the arteriole occurred either by diffusion through extracellular space (diffusion curves) or by both K⁺ siphoning through astrocytes and diffusion (diffusion and siphoning curves). (A) The imposed [K⁺]_o increase was distributed uniformly throughout the brain (beginning 2.5 μm from the arteriole). (B) The imposed [K⁺]_o increase began a distance of 50 μm from the arteriole. Insets illustrate the geometry of the model system and the initial distribution of the imposed [K⁺]_o increase (shaded region). In both (A) and (B) [K⁺] at the arteriole increased more rapidly and to a higher level when diffusion was augmented by K⁺ siphoning.