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Prostaglandin E 2 , a postulated astrocyte‐derived neurovascular coupling agent, constricts rather than dilates parenchymal arterioles
Author(s) -
Dabertrand Fabrice,
Hannah Rachael M,
Pearson Jessica M,
HillEubanks David C,
Brayden Joseph E,
Nelson Mark T
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.880.4
Subject(s) - neurovascular bundle , parenchyma , vasoconstriction , arteriole , receptor , prostaglandin e , prostaglandin , endocrinology , medicine , prostanoid , anatomy , biology , microcirculation , chemistry , pathology
Prostaglandin E 2 (PGE 2 ) is proposed to be 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. Particularly, PGE 2 is the most versatile of the prostaglandins because of four different receptors subtypes linked to opposing pathways in smooth muscle cells. 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 (11.7%, 18.6% and 34.3%, respectively) 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. Supported by AHA 09POST2290090 (FD), the NIH R37DK053832, PO1 HL095488, RO1HL44455, RO1HL58231, the Totman Trust for Medical Research and the Fondation Leducq for the Transatlantic Network of Excellence on the Pathogenesis of Small Vessel Disease of the Brain.