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N-arachidonoyl glycine suppresses Na+/Ca2+ exchanger-mediated Ca2+ entry into endothelial cells and activates BKCa channels independently of GPCRs

机译：N-花生四烯酸甘氨酸抑制Na + / Ca2 +交换子介导的Ca2 +进入内皮细胞并独立于GPCR激活BKCa通道

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摘要

Background and PurposeN-arachidonoyl glycine (NAGly) is a lipoamino acid with vasorelaxant properties. We aimed to explore the mechanisms of NAGly's action on unstimulated and agonist-stimulated endothelial cells.

机译：背景和目的N-花生四烯酰基甘氨酸（NAGly）是一种具有血管舒张特性的脂氨基酸。我们旨在探讨NAGly对未刺激和激动剂刺激的内皮细胞的作用机制。

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期刊名称 British Journal of Pharmacology and Chemotherapy
作者
Alexander I Bondarenko; Konstantin Drachuk; Olga Panasiuk; Vadim Sagach; Andras T Deak; Roland Malli; Wolfgang F Graier;
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作者单位

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年(卷),期 2013(169),4
年度 2013
页码 933–948
总页数 16
原文格式 PDF
正文语种
中图分类药学 ;
关键词
N-arachidonoyl glycine endothelial Nasup+/sup/Casup2+/sup exchanger membrane potential acetylcholine histamine BKCa channels;

机译：N-花生四烯酸甘氨酸;内皮;Na sup + / sup / Ca sup 2 + / sup交换子;膜电位;乙酰胆碱;组胺;BKCa通道;

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专利

1. Extracellular acidosis suppresses endothelial function by inhibiting store-operated Ca2+ entry via non-selective cation channels. [J] . Asai M, Takeuchi K, Saotome M Cardiovascular Research . 2009 ,第1期

机译：细胞外酸中毒通过抑制存储操纵的Ca2 +通过非选择性阳离子通道的进入来抑制内皮功能。
2. Extracellular acidosis suppresses endothelial function by inhibiting store-operated Ca2+ entry via non-selective cation channels [J] . Masayoshi Asai1 Kazuhiko Takeuchi2 Masao Saotome1 Tsuyoshi Urushida1 Hideki Katoh1 Hiroshi Satoh1 Hideharu Hayashi1 and Hiroshi Watanabe2* Cardiovascular Research . 2009 ,第1期

机译：细胞外酸中毒通过抑制存储操纵的Ca 2 + 通过非选择性阳离子通道的进入来抑制内皮功能
3. Activation of canonical transient receptor potential channels preserves Ca2+ entry and endothelium-derived hyperpolarizing factor-mediated function in vitro in porcine coronary endothelial cells and coronary arteries under conditions of hyperkalemia [J] . YangQ., HuangJ.-H., YaoX.-Q., The Journal of Thoracic and Cardiovascular Surgery . 2014 ,第4期

机译：在高钾血症条件下，猪冠状动脉内皮细胞和冠状动脉中，规范的瞬时受体电位通道的激活可在体外保留Ca2 +进入和内皮源的超极化因子介导的功能。
4. Ca2+ homeostasis in microvascular endothelial cells from an insulin-dependent diabetic model: role of endosomes/lysosomes [C] . Shankar C. Sanka, Texas Tech Univ. Health Sciences Ctr., Lubbock, Molecular Imaging: Reporters, Dyes, Markers, and Instrumentation . 2000

机译：胰岛素依赖型糖尿病模型中微血管内皮细胞中的Ca2 +稳态：内体/溶酶体的作用
5. Studies on Endothelial cell -Ca2+ - or Mg2+ -ATPase and Plasminogen Activator- [D] . 萩原啓実. 1984

机译：内皮细胞-Ca2 +-或Mg2 + -ATPase和纤溶酶原激活物的研究
6. The whole‐cell Ca2+ release‐activated Ca2+ current ICRAC is regulated by the mitochondrial Ca2+ uniporter channel and is independent of extracellular and cytosolic Na+ [O] . Krishna Samanta, Daniel Bakowski, Nader Amin, -1

机译：全细胞Ca2 +释放激活的Ca2 +电流ICRAC受线粒体Ca2 +单向通道调控独立于细胞外和胞质Na +
7. Evidence for a receptor-activated Ca2+ entry pathway independent from Ca2+ store depletion in endothelial cells [O] . H. Jousset, R. Malli, N. Girardin, 2008

机译：受体激活的CA2 +进入途径的证据与内皮细胞中的CA2 +储存耗尽无关

N-arachidonoyl glycine suppresses Na+/Ca2+ exchanger-mediated Ca2+ entry into endothelial cells and activates BKCa channels independently of GPCRs

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