Cellular signal transduction by anandamide and 2-arachidonoylglycerol

Chem Phys Lipids. 2000 Nov;108(1-2):53-70. doi: 10.1016/s0009-3084(00)00187-0.


Anandamide (arachidonylethanolamide) and 2-arachidonoylglycerol mediate many of their actions via either CB(1) or CB(2) cannabinoid receptor subtypes. These agonist-receptor interactions result in activation of G proteins, particularly those of the G(i/o) family. Signal transduction pathways that are regulated by these G proteins include inhibition of adenylyl cyclase, regulation of ion currents (inhibition of voltage-gated L, N and P/Q Ca(2+)-currents; activation of K(+) currents); activation of focal adhesion kinase (FAK), mitogen activated protein kinase (MAPK) and induction of immediate early genes; and stimulation of nitric oxide synthase (NOS). Other effects of anandamide and/or 2-arachidonoylglycerol that are not mediated via cannabinoid receptors include inhibition of L-type Ca(2+) channels, stimulation of VR(1) vanilloid receptors, transient changes in intracellular Ca(2+), and disruption of gap junction function. Cardiovascular regulation by anandamide appears to occur by a variety of receptor-mediated and non-receptor-mediated mechanisms. This review will describe and evaluate each of these signal transduction pathways and mechanisms.

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Arachidonic Acids / pharmacology*
  • Calcium / metabolism
  • Endocannabinoids
  • Gap Junctions / drug effects
  • Glycerides / pharmacology*
  • Humans
  • Polyunsaturated Alkamides
  • Receptors, Cannabinoid
  • Receptors, Drug / drug effects
  • Signal Transduction / drug effects*


  • Arachidonic Acids
  • Endocannabinoids
  • Glycerides
  • Polyunsaturated Alkamides
  • Receptors, Cannabinoid
  • Receptors, Drug
  • glyceryl 2-arachidonate
  • Calcium
  • anandamide