Department of Physiology, Semmelweis University, Budapest, Hungary.
Mol Cell Endocrinol. 2012 Apr 28;353(1-2):29-36. doi: 10.1016/j.mce.2011.10.011. Epub 2011 Nov 2.
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 G(q/11) proteins and, in some cases, G(s) 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 AT(1) receptors, similar to other G(q/11)-coupled receptors, can lead to the formation of 2-arachidonoylglycerol (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 CB(1) cannabinoid receptors (CB(1)Rs). We conclude that activation of the ECS should be considered as a general consequence of the stimulation of G(q/11)-coupled receptors, and may mediate some of the physiological effects of GPCRs.
在过去的几年中，内源性大麻素系统（ECS）与其他激素和神经调制系统之间的关系已得到深入研究。G 蛋白偶联受体（GPCR）可通过激活 G(q/11)蛋白，在某些情况下通过 G(s)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 激活触发 eCB 释放的途径，以及在全身组织中这一过程的一些最为人熟知的例子。血管紧张素 II 诱导的 AT(1)受体激活，与其他 G(q/11)偶联受体相似，可导致 2-花生四烯酸甘油（2-AG）的形成，这是一种重要的 eCB。血管紧张素 II 直接注射到麻醉大鼠下丘脑室旁核引起的高血压效应可被 AM251 （CB(1)大麻素受体的反向激动剂）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。我们得出结论，ECS 的激活应被视为 G(q/11)偶联受体刺激的一般后果，并且可能介导 GPCR 的一些生理效应。
