The Obligatory Role of the Acetylcholine-Induced Endothelium-Dependent Contraction in Hypertension: Can Arachidonic Acid Resolve this Inflammation?
The Obligatory Role of the Acetylcholine-Induced Endothelium-Dependent Contraction in Hypertension: Can Arachidonic Acid Resolve this Inflammation?
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DOI：
10.2174/1381612826666200417150121
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发表时间：
2020
影响因子：
3.1
通讯作者：
Wenceslau CF
中科院分区：
文献类型：
--
作者：
Edwards JM;McCarthy CG;Wenceslau CF
内皮细胞产生许多可以调节血管张力的物质。乙酰胆碱是一种广泛使用的评估内皮功能的药理学工具。一般来说，乙酰胆碱与G蛋白偶联的M受体结合，介导细胞内游离钙的一过性升高。这种细胞内钙的升高负责触发几种细胞反应，包括一氧化氮、内皮衍生的超极化因子和花生四烯酸衍生的二十烷基类化合物的合成。内皮花生四烯酸代谢也是介导炎症反应的重要信号通路。因此，在持续和过度炎症的情况下，如高血压，花生四烯酸作为合成几种收缩血管的代谢物的底物，主要通过环氧合酶和脂氧合酶。然后，环氧合酶和脂氧合酶产物可以激活血管平滑肌细胞上表达的G蛋白偶联受体，从而引起收缩反应。因此，由花生四烯酸引起的乙酰胆碱引起的收缩是高血压患者血管内皮功能障碍和血管炎症的常见特征。在这篇综述中，我们将批判性地分析支持这一概念的文献，以及潜在的潜在机制，包括在高血压等条件下花生四烯酸信号从合成促分解代谢物转移的可能性。
The endothelium produces many substances that can regulate vascular tone. Acetylcholine is a widely used pharmacological tool to assess endothelial function. In general, acetylcholine binds to G-protein coupled muscarinic receptors that mediate a transient elevation in intracellular, free calcium. This intracellular rise in calcium is responsible for triggering several cellular responses, including the synthesis of nitric oxide, endothelium-derived hyperpolarizing factor, and eicosanoids derived from arachidonic acid. Endothelial arachidonic acid metabolism is also an important signaling pathway for mediating inflammation. Therefore, in conditions with sustained and excessive inflammation such as hypertension, arachidonic acid serves as a substrate for the synthesis of several vasoconstrictive metabolites, predominantly via the cyclooxygenase and lipoxygenase enzymes. Cyclooxygenase and lipoxygenase products can then activate G-protein coupled receptors expressed on vascular smooth muscle cells to causes contractile responses. As a result, acetylcholine-induced contraction due to arachidonic acid is a commonly observed feature of endothelial dysfunction and vascular inflammation in hypertension. In this review, we will critically analyze the literature supporting this concept, as well as address the potential underlying mechanisms, including the possibility that arachidonic acid signaling is diverted away from the synthesis of pro-resolving metabolites in conditions such as hypertension.
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影响因子：
20.1
作者：
Chen, GF;Cheung, DW
通讯作者：
Cheung, DW
影响因子：
30.5
作者：
Haworth, Oliver;Cernadas, Manuela;Levy, Bruce D.
通讯作者：
Levy, Bruce D.
影响因子：
12.3
作者：
DelliPizzi, A;Guan, H;Nasjletti, A
通讯作者：
Nasjletti, A
DOI：
10.1152/ajpheart.01115.2005
发表时间：
2006-11-01
影响因子：
4.8
作者：
Gluais, Pascale;Paysant, Jerome;Feletou, Michel
通讯作者：
Feletou, Michel
影响因子：
5
作者：
Gluais, Pascale;Vanhoutte, Paul M.;Feletou, Michel
通讯作者：
Feletou, Michel