Abstract
Marijuana is used by humans for its psychoactive and medicinal effects. The active constituents of marijuana, the cannabinoids, exert effects via a G protein-coupled receptor, CB1. Two arachidonic acid analogs, N-arachidonylethanolamine and 2-arachidonylglycerol are hypothesized to function as endogenous ligands of the CB1 receptor. The cannabinoids exert significant vascular effects in humans and laboratory animals. In particular, the cannabinoids produce vasodilation and hypotension. The possible mechanisms for these effects are inhibition of transmitter release from sympathetic nerve terminals, direct effects on vascular smooth muscle cells, and effects on endothelial cell function. The data regarding these effects of the cannabinoids and possible sources of endocannabinoid ligands in the vasculature are the subjects of this review.
Footnotes
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↵1 The author was supported by National Institutes of Health Grants DA09155 and DA08098 during the writing of this review.
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Received for publication January 31, 2000.
- Abbreviations:
- Δ9-THC
- Δ9-tetrahydrocannabinol
- AEA
- N-arachidonylethanolamine
- 2-AG
- 2-arachidonylglycerol
- CB1
- neuronal cannabinoid receptor
- CNS
- central nervous system
- DMHP
- 1-hydroxy-3(1,2-dimethylheptyl)-6,6,9-trimethyl 7,8,9,10-tetrahydro-6-dibenzopyran
- EDHF
- endothelial-derived hyperpolarizing factor
- NO
- nitric oxide
- Accepted February 23, 2000.
- The American Society for Pharmacology and Experimental Therapeutics
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