Lack of involvement of pertussis toxin-sensitive G-proteins in norepinephrine-induced vasoconstriction of rat aorta smooth muscle11Abbreviations: α-AR, α-adrenoceptor; DTT, dl-dithiothreitol; NE, norepinephrine; PSS, physiological salt solution; PTX, pertussis-toxin; and SMC, smooth muscle cells.

Background and purpose: Studies in isolated preparations of vascular tissue (mainly resistance vessels) provide evidence that anandamide exerts vasorelaxation. The aim of the present work was to further characterize the mechanisms involved in the vascular response induced by anandamide in a conduit vessel, rat aorta. Experimental approach: Isometric tension changes in response to a cumulative concentration-response curve of anandamide (1 nM-100 mM) were recorded in aortic rings from male Wistar rats. The involvement of a number of factors in this relaxation was investigated including endothelium-derived vasorelaxant products, cannabinoid and vanilloid receptors (transient potential vanilloid receptor-1 (TRPV1)), release of calcitonin gene-related peptide (CGRP), anandamide metabolism and the membrane transporter for anandamide. Key results: Anandamide caused a significant concentration-dependent vasorelaxation in rat aorta. This vasorelaxation was significantly inhibited by Pertussis toxin, by a non-CB 1 /non-CB 2 cannabinoid receptor antagonist, by endothelial denudation, by inhibition of nitric oxide synthesis or inhibition of prostanoid synthesis via cyclooxygenase-2 (COX-2), by blockade of prostaglandin receptors EP 4 and by a fatty acid amino hydrolase inhibitor. Antagonists for CB 1 , CB 2 , TRPV1 or CGRP receptors, an inhibitor of the release of endothelium-derived hyperpolarizing factor, and an inhibitor of anandamide transport did not modify the vascular response to anandamide. Conclusions and implications: Our results demonstrate, for the first time, the involvement of the non-CB1/non-CB2 cannabinoid receptor and an anandamide-arachidonic acid-COX-2 derived metabolite (which acts on EP 4 receptors) in the endothelial vasorelaxation caused by anandamide in rat aorta.

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Lack of involvement of pertussis toxin-sensitive G-proteins in norepinephrine-induced vasoconstriction of rat aorta smooth muscle11Abbreviations: α-AR, α-adrenoceptor; DTT, dl-dithiothreitol; NE, norepinephrine; PSS, physiological salt solution; PTX, pertussis-toxin; and SMC, smooth muscle cells.

Cited by 9 publications

References 26 publications

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Pertussis toxin-induced histamine sensitisation: an aspecific phenomenon independent from the nitric oxide system?

Role of Gi-proteins in norepinephrine-mediated vasoconstriction in rat tail artery smooth muscle

Characterization of the vasorelaxant mechanisms of the endocannabinoid anandamide in rat aorta

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