Abstract
Cannabinoids (natural, endogenous and synthetic compounds) produce vasorelaxation in resistance and conduit arteries. Several putative mechanisms have been proposed to explain this effect of cannabinoids. The aim of the present review is to discuss the different mechanisms involved in the vasorelaxant effect of endogenous and synthetic cannabinoids in resistance and conduit arteries. Research on the vascular effects of cannabinoids suggests that the magnitude of the vasorelaxation and the mechanisms involved are not identical in all vascular beds with one or two mechanisms predominating. Either extracellular or intracellular mechanisms are involved. With regard to the former, the stimulation of cannabinoid CB1, CB2 or nonCB1/nonCB2 cannabinoid receptors and the stimulation of vanilloid receptors, transient potential vanilloid receptors, on perivascular nerve endings with the subsequent release of the vasodilator neurotransmitter calcitonin gene-related peptide have been described. With regard to the latter, the main mechanisms implicated include nitric oxide release, metabolism to vasoactive arachidonic metabolites or prostanoid analogues, or endothelium derived hyperpolarising factor release. The knowledge of these mechanisms is crucial to identify new therapeutic targets and to understand the consequences in different vascular beds.
Keywords: Cannabinoids, blood vessels, vasorelaxation, mechanisms
Current Vascular Pharmacology
Title: Vasorelaxation Caused by Cannabinoids: Mechanisms in Different Vascular Beds
Volume: 6 Issue: 4
Author(s): Visitacion Lopez-Miranda, Esperanza Herradon and M Isabel Martin
Affiliation:
Keywords: Cannabinoids, blood vessels, vasorelaxation, mechanisms
Abstract: Cannabinoids (natural, endogenous and synthetic compounds) produce vasorelaxation in resistance and conduit arteries. Several putative mechanisms have been proposed to explain this effect of cannabinoids. The aim of the present review is to discuss the different mechanisms involved in the vasorelaxant effect of endogenous and synthetic cannabinoids in resistance and conduit arteries. Research on the vascular effects of cannabinoids suggests that the magnitude of the vasorelaxation and the mechanisms involved are not identical in all vascular beds with one or two mechanisms predominating. Either extracellular or intracellular mechanisms are involved. With regard to the former, the stimulation of cannabinoid CB1, CB2 or nonCB1/nonCB2 cannabinoid receptors and the stimulation of vanilloid receptors, transient potential vanilloid receptors, on perivascular nerve endings with the subsequent release of the vasodilator neurotransmitter calcitonin gene-related peptide have been described. With regard to the latter, the main mechanisms implicated include nitric oxide release, metabolism to vasoactive arachidonic metabolites or prostanoid analogues, or endothelium derived hyperpolarising factor release. The knowledge of these mechanisms is crucial to identify new therapeutic targets and to understand the consequences in different vascular beds.
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Cite this article as:
Lopez-Miranda Visitacion, Herradon Esperanza and Martin Isabel M, Vasorelaxation Caused by Cannabinoids: Mechanisms in Different Vascular Beds, Current Vascular Pharmacology 2008; 6 (4) . https://dx.doi.org/10.2174/157016108785909706
DOI https://dx.doi.org/10.2174/157016108785909706 |
Print ISSN 1570-1611 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-6212 |
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