Calignano A, La Rana G, Makriyannis A, Lin S Y, Beltramo M, Piomelli D
Department of Experimental Pharmacology, University of Naples, Italy.
Eur J Pharmacol. 1997 Dec 11;340(2-3):R7-8.
The endogenous cannabinoid ligand anandamide (arachidonylethanolamide) inhibited the intestinal passage of a charcoal meal when administered s.c. in mice at doses ranging from 0.1 to 50 mg/kg. This effect was prevented by the cannabinoid CB1 receptor antagonist SR141716A [N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-me thyl-1H-pyrazole-3-carboxamide x HCl] (1 mg/kg s.c.), but it was not affected by the anandamide transport inhibitor, N-(4-hydroxyphenyl) arachidonylethanolamide (AM404) (50 mg/kg, s.c.). The results indicate that anandamide modulates intestinal motility in mice by activating cannabinoid CB1 receptors. They also suggest that anandamide transport, which was previously shown to participate in terminating neural and vascular responses to anandamide, does not contribute to anandamide inactivation in intestinal tissue.
内源性大麻素配体花生四烯酸乙醇胺（anandamide）以0.1至50mg/kg的剂量皮下注射给小鼠时，会抑制炭末在肠道中的推进。大麻素CB1受体拮抗剂SR141716A [N-（哌啶-1-基）-5-（4-氯苯基）-1-（2,4-二氯苯基）-4-甲基-1H-吡唑-3-甲酰胺×HCl]（1mg/kg皮下注射）可阻止这种作用，但它不受花生四烯酸乙醇胺转运抑制剂N-（4-羟基苯基）花生四烯酸乙醇胺（AM404）（50mg/kg，皮下注射）的影响。结果表明，花生四烯酸乙醇胺通过激活大麻素CB1受体来调节小鼠的肠道运动。它们还表明，先前已证明参与终止对花生四烯酸乙醇胺的神经和血管反应的花生四烯酸乙醇胺转运，在肠道组织中对花生四烯酸乙醇胺的失活没有作用。
