Astrocytic endfoot Ca2+ and BK channels determine both arteriolar dilation and constriction

Proc Natl Acad Sci U S A. 2010 Feb 23;107(8):3811-6. doi: 10.1073/pnas.0914722107. Epub 2010 Feb 2.


Neuronal activity is thought to communicate to arterioles in the brain through astrocytic calcium (Ca(2+)) signaling to cause local vasodilation. Paradoxically, this communication may cause vasoconstriction in some cases. Here, we show that, regardless of the mechanism by which astrocytic endfoot Ca(2+) was elevated, modest increases in Ca(2+) induced dilation, whereas larger increases switched dilation to constriction. Large-conductance, Ca(2+)-sensitive potassium channels in astrocytic endfeet mediated a majority of the dilation and the entire vasoconstriction, implicating local extracellular K(+) as a vasoactive signal for both dilation and constriction. These results provide evidence for a unifying mechanism that explains the nature and apparent duality of the vascular response, showing that the degree and polarity of neurovascular coupling depends on astrocytic endfoot Ca(2+) and perivascular K(+).

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Arterioles / drug effects
  • Arterioles / innervation
  • Arterioles / physiology*
  • Astrocytes / metabolism*
  • Brain / blood supply
  • Calcium / pharmacology
  • Calcium / physiology
  • Calcium Signaling*
  • Cerebrovascular Circulation
  • Large-Conductance Calcium-Activated Potassium Channels / metabolism*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Neurons / metabolism
  • Potassium / pharmacology
  • Vasoconstriction*
  • Vasodilation*


  • Large-Conductance Calcium-Activated Potassium Channels
  • Potassium
  • Calcium