Department of Pharmacology, College of Medicine, University of Vermont, Burlington, VT 05405-0068, USA.
J Cereb Blood Flow Metab. 2013 Apr;33(4):479-82. doi: 10.1038/jcbfm.2013.9. Epub 2013 Feb 6.
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.
有人提出，在神经血管耦联期间，前列腺素 E2（PGE2）从星形胶质细胞终足释放出来，通过激活前列腺素（EP4）受体来扩张实质小动脉。然而，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 对来自大鼠和小鼠脑的分离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 5 μmol/L）收缩而不是扩张实质小动脉。EP1 受体抑制剂可防止 PGE2 引起的血管收缩。这些结果强烈反对 PGE2 在神经血管耦联期间对小动脉的直接作用。
