Regulation of endocannabinoid release by G proteins: A paracrine mechanism of G protein-coupled receptor action

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• 作者：Pá ; l Gyombolai^a ; Dorottya Pap^b ; Gá ; bor Turu^a ; Kevin J. Catt^c ; Gyö ; rgy Bagdy^b ; ^d ; Lá ; szló ; Hunyady^a ; ^e ; ^{hunyady@eok.sote.hu}
• 关键词：Endocannabinoid ; CB1 ; GPCR ; Angiotensin II
• 刊名：Molecular and Cellular Endocrinology
• 出版年：2012
• 期刊代码：109_03037207
• 类别：bio
• 出版时间：28 April, 2012
• 卷：353
• 期：1-2
• 页码：29-36
• 文件大小：417 K

摘要

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 AT₁ 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 CB₁ cannabinoid receptors (CB₁Rs). 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.