Prostaglandin E2, a Postulated Astrocyte-Derived Neurovascular Coupling Agent, Constricts Rather than Dilates Parenchymal Arterioles | Zendy

Fabrice Dabertrand | Zendy; Rachael M. Hannah | Zendy; J.M. Pearson | Zendy; David C. HillEubanks | Zendy; Joseph E. Brayden | Zendy; Mark T. Nelson | Zendy

Open Access

Prostaglandin E₂, a Postulated Astrocyte-Derived Neurovascular Coupling Agent, Constricts Rather than Dilates Parenchymal Arterioles

Author(s) -

Fabrice Dabertrand,

Rachael M. Hannah,

J.M. Pearson,

David C. HillEubanks,

Joseph E. Brayden,

Mark T. Nelson

Publication year - 2013

Publication title -

journal of cerebral blood flow and metabolism

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.167

H-Index - 193

eISSN - 1559-7016

pISSN - 0271-678X

DOI - 10.1038/jcbfm.2013.9

Subject(s) - neurovascular bundle , parenchyma , vasoconstriction , arteriole , astrocyte , prostaglandin , prostaglandin e , receptor , anatomy , prostanoid , endocrinology , medicine , microcirculation , biology , chemistry , pathology , central nervous system

It has been proposed that prostaglandin E 2 (PGE 2 ) is released from astrocytic endfeet to dilate parenchymal arterioles through activation of prostanoid (EP 4 ) receptors during neurovascular coupling. However, the direct effects of PGE 2 on isolated parenchymal arterioles have not been tested. Here, we examined the effects of PGE 2 on the diameter of isolated pressurized parenchymal arterioles from rat and mouse brain. Contrary to the prevailing assumption, we found that PGE 2 (0.1, 1, and 5 μmol/L) constricted rather than dilated parenchymal arterioles. Vasoconstriction to PGE 2 was prevented by inhibitors of EP 1 receptors. These results strongly argue against a direct role of PGE 2 on arterioles during neurovascular coupling.

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