首页> 美国卫生研究院文献>Journal of Cerebral Blood Flow Metabolism >Prostaglandin E2 a postulated astrocyte-derived neurovascular coupling agent constricts rather than dilates parenchymal arterioles
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Prostaglandin E2 a postulated astrocyte-derived neurovascular coupling agent constricts rather than dilates parenchymal arterioles

机译:假定的星形胶质细胞衍生的神经血管偶联剂前列腺素E2收缩而不是扩张实质小动脉

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摘要

It has been proposed that prostaglandin E2 (PGE2) is released from astrocytic endfeet to dilate parenchymal arterioles through activation of prostanoid (EP4) receptors during neurovascular coupling. However, the direct effects of PGE2 on isolated parenchymal arterioles have not been tested. Here, we examined the effects of PGE2 on the diameter of isolated pressurized parenchymal arterioles from rat and mouse brain. Contrary to the prevailing assumption, we found that PGE2 (0.1, 1, and 5 μmol/L) constricted rather than dilated parenchymal arterioles. Vasoconstriction to PGE2 was prevented by inhibitors of EP1 receptors. These results strongly argue against a direct role of PGE2 on arterioles during neurovascular coupling.
机译:已经提出,前列腺素E2(PGE2)从星形胶质细胞的末端释放,通过在神经血管偶联过程中激活前列腺素(EP4)受体来扩张实质小动脉。但是,尚未测试PGE2对分离的实质小动脉的直接作用。在这里,我们检查了PGE2对大鼠和小鼠脑中分离的加压实质小动脉直径的影响。与普遍的假设相反,我们发现PGE2(0.1、1和5μmol/ L)收缩而不是扩张的实质小动脉。 EP1受体抑制剂可预防PGE2的血管收缩。这些结果强烈反对了PGE 2在神经血管偶联过程中对小动脉的直接作用。

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