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血管加压素通过钙刺激的磷脂酶A2介导,刺激A7r5血管平滑肌细胞中花生四烯酸的释放。

Stimulation of arachidonic acid release by vasopressin in A7r5 vascular smooth muscle cells mediated by Ca2+-stimulated phospholipase A2.

作者信息

Liu Yingjie, Taylor Colin W

机构信息

Department of Pharmacology, Tennis Court Road, Cambridge CB2 1PD, UK.

出版信息

FEBS Lett. 2006 Jul 24;580(17):4114-20. doi: 10.1016/j.febslet.2006.06.055. Epub 2006 Jun 30.

Abstract

Arachidonic acid (AA) regulates many aspects of vascular smooth muscle behaviour, but the mechanisms linking receptors to AA release are unclear. In A7r5 vascular smooth muscle cells pre-labelled with (3)H-AA, vasopressin caused a concentration-dependent stimulation of 3H-AA release that required phospholipase C and an increase in cytosolic [Ca2+]. Ca2+ release from intracellular stores and Ca2+ entry via L-type channels or the capacitative Ca2+ entry pathway were each effective to varying degrees. Selective inhibitors of PLA2 inhibited the 3H-AA release evoked by vasopressin, though not the underlying Ca2+ signals, and established that cPLA2 mediates the release of AA. We conclude that in A7r5 cells vasopressin stimulates AA release via a Ca2+-dependent activation of cPLA2.

摘要

花生四烯酸(AA)调节血管平滑肌行为的多个方面,但其将受体与AA释放联系起来的机制尚不清楚。在预先用(3)H-AA标记的A7r5血管平滑肌细胞中,血管加压素引起了3H-AA释放的浓度依赖性刺激,这需要磷脂酶C和胞质[Ca2+]的增加。从细胞内储存释放Ca2+以及通过L型通道或容量性Ca2+内流途径进入Ca2+均在不同程度上有效。PLA2的选择性抑制剂抑制了血管加压素引起的3H-AA释放,尽管没有抑制潜在的Ca2+信号,并证实cPLA2介导AA的释放。我们得出结论,在A7r5细胞中,血管加压素通过cPLA2的Ca2+依赖性激活刺激AA释放。

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