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Prostaglandin E2, a postulated astrocyte-derived neurovascular coupling agent, constricts rather than dilates parenchymal arterioles.


ABSTRACT: 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 ?mol/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.

SUBMITTER: Dabertrand F 

PROVIDER: S-EPMC3618402 | biostudies-literature | 2013 Apr

REPOSITORIES: biostudies-literature

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Prostaglandin E2, a postulated astrocyte-derived neurovascular coupling agent, constricts rather than dilates parenchymal arterioles.

Dabertrand Fabrice F   Hannah Rachael M RM   Pearson Jessica M JM   Hill-Eubanks David C DC   Brayden Joseph E JE   Nelson Mark T MT  

Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 20130206 4


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, an  ...[more]

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