http://cshperspectives.cshlp.org/content/early/2015/03/27/cshperspect.a020388.abstract
Abstract
Neuronal activity results in increased blood flow in the brain, a response named functional hyperemia. Astrocytes play an
important role in mediating this response. Neurotransmitters released from active neurons evoke Ca2+
increases in astrocytes, leading to the release of vasoactive
metabolites of arachidonic acid from astrocyte endfeet onto
blood vessels. Synthesis of prostaglandin E2 (PGE2)
and epoxyeicosatrienoic acids (EETs) dilate blood vessels, whereas
20-hydroxyeicosatetraenoic
acid (20-HETE) constricts vessels. The release of K+ from astrocyte endfeet may also contribute to vasodilation. Oxygen modulates astrocyte regulation of blood flow. Under normoxic
conditions, astrocytic Ca2+ signaling
results in vasodilation, whereas under hyperoxic conditions,
vasoconstriction is favored. Astrocytes also contribute
to the generation of vascular tone. Tonic release
of both 20-HETE and ATP from astrocytes constricts vascular smooth
muscle
cells, generating vessel tone. Under pathological
conditions, including Alzheimer’s disease and diabetic retinopathy,
disruption
of normal astrocyte physiology can compromise the
regulation of blood flow.
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