Regulation of endocannabinoid release by G proteins: a paracrine mechanism of G protein-coupled receptor action.
Regulation of endocannabinoid release by G proteins: a paracrine mechanism of G protein-coupled receptor action.
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DOI：
10.1016/j.mce.2011.10.011
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发表时间：
2012-04-28
影响因子：
4.1
通讯作者：
Hunyady, Laszlo
中科院分区：
文献类型：
--
作者：
Gyombolai, Pal;Pap, Dorottya;Turu, Gabor;Catt, Kevin J.;Bagdy, Gyoergy;Hunyady, Laszlo
在过去的几年里，内源性大麻素系统(ECS)与其他激素和神经调节系统之间的关系得到了广泛的研究。G蛋白偶联受体(GPCRs)可通过激活Gq/11蛋白和某些情况下的Gs蛋白来刺激内源性大麻素(ECB)的产生。在这篇综述中，我们总结了GPCR激活可以触发ECB释放的途径，以及整个身体组织中这一过程的最著名的例子。与其他GQ/11偶联受体类似，血管紧张素II诱导的AT1受体的激活可导致重要的ECB-2-花生四烯基诺甘油(2-AG)的形成。直接注射到麻醉大鼠下丘脑室旁核的血管紧张素II的升压效应可以被CB1大麻受体(CB1Rs)的反向激动剂AM251消除，这一发现支持了ECB形成在血管紧张素II作用中的重要性。我们的结论是，ECS的激活应被认为是刺激GQ/11偶联受体的一般结果，并可能介导GPCRs的某些生理效应。
In the past years, the relationship between the endocannabinoid system (ECS) and other hormonal and neuromodulatory systems has been intensively studied. G protein-coupled receptors (GPCRs) can stimulate endocannabinoid (eCB) production via activation of Gq/11 proteins and, in some cases, Gs proteins. In this review, we summarize the pathways through which GPCR activation can trigger eCB release, as well as the best known examples of this process throughout the body tissues. Angiotensin II-induced activation of AT1 receptors, similar to other Gq/11-coupled receptors, can lead to the formation of 2-arachido-noylglycerol (2-AG), an important eCB. The importance of eCB formation in angiotensin II action is supported by the finding that the hypertensive effect of angiotensin II, injected directly into the hypothalamic paraventricular nucleus of anaesthetized rats, can be abolished by AM251, an inverse agonist of CB1 cannabinoid receptors (CB1Rs). We conclude that activation of the ECS should be considered as a general consequence of the stimulation of Gq/11-coupled receptors, and may mediate some of the physiological effects of GPCRs.
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影响因子：
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