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Am J Physiol Heart Circ Physiol 282: H2046-H2054, 2002. First published January 24, 2002; doi:10.1152/ajpheart.00497.2001
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Vol. 282, Issue 6, H2046-H2054, June 2002

Anandamide-induced vasorelaxation in rabbit aortic rings has two components: G protein dependent and independent

Somnath Mukhopadhyay, Barry M. Chapnick, and Allyn C. Howlett

Department of Pharmacological and Physiological Science, St. Louis University School of Medicine, St. Louis, Missouri 63104

The endogenous cannabinoid anandamide (arachidonylethanolamide) produces vasorelaxation in different vascular beds. In the present study, we found that anandamide and a metabolically stable analog, methanandamide, produced dose-dependent (10 nM-10 µM) vasorelaxation of ~80% in a rabbit aortic ring preparation in an endothelium-dependent manner. Non-endothelium-dependent vasorelaxation was observed to be a maximum of 20-22% at >10 µM methanandamide. The efficacious CB1 receptor analogs desacetyllevonantradol (10 µM) and WIN55212-2 (10 µM) failed to produce vasorelaxation; however, the endothelium-dependent vasorelaxation evoked by methanandamide was partially (75%) blocked by the CB1 receptor antagonist SR141716A. The VR1 vanilloid receptor antagonist capsazepine or the calcitonin gene-related peptide (CGRP) antagonist CGRP-(8-37) partially attenuated (25%) the vasorelaxation in endothelium-intact preparations and greatly reduced the response in endothelium-denuded preparations. Pretreatment of aortic rings with NG-nitro-L-arginine methyl ester completely blocked the methanandamide-, capsaicin-, and CGRP-induced vasorelaxation. Pretreatment of aortic rings with pertussis toxin attenuated the methanandamide-induced vasorelaxation in endothelium-intact aortic rings, indicating the involvement of Gi/o proteins in the vasorelaxation; however, pertussis toxin treatment failed to block the endothelium-independent response. Thus, in the rabbit aorta, methanandamide-induced vasorelaxation exhibits two components: 1) in endothelium-intact rings, an SR141716A-sensitive, non-CB1 receptor component that requires pertussis toxin-sensitive G proteins and nitric oxide (NO) production; and 2) in endothelium-denuded rings, a component that is mediated by VR1 vanilloid receptors and possibly by the subsequent release of CGRP that requires NO production but is independent of pertussis toxin-sensitive G proteins.

cannabinoid receptors; vanilloid receptors; pertussis toxin; endothelium; nitric oxide


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