The DOI matches its Crossref record; 3 of the 3 references it cites were found in a registry or an index.
Astrocyte control of the cerebrovasculature
Abstract
The control of cerebral vessel diameter is of fundamental importance in maintaining healthy brain function because it is critical to match cerebral blood flow (CBF) to the metabolic demand of active neurons. Recent studies have shown that astrocytes are critical players in the regulation of cerebral blood vessel diameter and that there are several molecular pathways through which astrocytes can elicit these changes. Increased intracellular Ca 2+ in astrocytes has demonstrated a dichotomy in vasomotor responses by causing the constriction as well as the dilation of neighboring blood vessels. The production of arachidonic acid (AA) in astrocytes by Ca 2+ sensitive phospholipase A 2 (PLA 2) has been shown to be common to both constriction and dilation mechanisms. Constriction results from the conversion of AA to 20‐hydroxyeicosatetraenoic acid (20‐HETE) and dilation from the production of prostaglandin E 2 (PGE2) or epoxyeicosatrienoic acid (EET) and the level of nitric oxide (NO) appears to dictate which of these two pathways is recruited. In addition the activation of Ca 2+ activated K+ channels in astrocyte endfeet and the efflux of K+ has also been suggested to modify vascular tone by hyperpolarization and relaxation of smooth muscle cells (SMCs). The wide range of putative pathways indicates that more work is needed to clarify the contributions of astrocytes to vascular dynamics under different cellular conditions. Nonetheless it is clear that astrocytes are important albeit complicated regulators of CBF. © 2007 Wiley‐Liss, Inc.
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Metadata
- Authors
- Gordon, G. R. J., Mulligan, S. J., & MacVicar, B. A.
- Venue
- Glia
- Publisher
- Wiley
- Published
- 2007-07-20
- Volume
- 55
- Issue
- 12
- Pages
- 1214-1221
- ISSN
- 0894-1491 (ISSN-L)
- 1098-1136
- OpenAlex
- W2100486119
- Cited by
- 321
- References
- 3
- FWCI
- 11.69
- Type
- journal article
- Language
- en
- Open access
- closed
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