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

被引：40

作者：

Dabertrand, Fabrice ^{[1
]}

Hannah, Rachael M. ^{[1
]}

Pearson, Jessica M. ^{[1
]}

Hill-Eubanks, David C. ^{[1
]}

Brayden, Joseph E. ^{[1
]}

Nelson, Mark T. ^{[1
,2
]}

机构：

[1] Univ Vermont, Coll Med, Dept Pharmacol, Burlington, VT 05405 USA

[2] Univ Manchester, Inst Cardiovasc Sci, Manchester, Lancs, England

来源：

JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM | 2013年 / 33卷 / 04期

基金：

美国国家卫生研究院;

关键词：

astrocytes; brain parenchymal arterioles; neurovascular coupling; prostaglandin E-2; CEREBRAL-CIRCULATION; BK CHANNELS; FUNCTIONAL HYPEREMIA; PROSTANOID RECEPTORS; EP2; RECEPTOR; BLOOD-FLOW; IN-VIVO; BRAIN; RESPONSES; VASODILATION;

D O I：

10.1038/jcbfm.2013.9

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

It has been proposed that prostaglandin E-2 (PGE(2)) is released from astrocytic endfeet to dilate parenchymal arterioles through activation of prostanoid (EP4) 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 mu mol/L) constricted rather than dilated parenchymal arterioles. Vasoconstriction to PGE(2) was prevented by inhibitors of EP1 receptors. These results strongly argue against a direct role of PGE(2) on arterioles during neurovascular coupling. Journal of Cerebral Blood Flow & Metabolism (2013) 33, 479-482; doi:10.1038/jcbfm.2013.9; published online 6 February 2013

引用

页码：479 / 482

页数：4

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