Plane F, Holland M, Waldron G J, Garland C J, Boyle J P
Department of Pharmacology, University of Bristol.
Br J Pharmacol. 1997 Aug;121(8):1509-11. doi: 10.1038/sj.bjp.0701361.
The endogenous cannabinoid, anandamide, has been suggested as an endothelium-derived hyperpolarizing factor (EDHF). We found that anandamide-evoked relaxation in isolated segments of rat mesenteric artery was associated with smooth muscle hyperpolarization. However, although anandamide-evoked relaxation was inhibited by either charybdotoxin (ChTX) or iberiotoxin, inhibition of the relaxation to EDHF required a combination of ChTX and apamin. The relaxations induced by either anandamide or EDHF were not inhibited by the cannabinoid receptor (CB1) antagonist SRI41716A, or mimicked by selective CB1 agonists. Thus, anandamide appears to cause smooth muscle relaxation via a CB1 receptor-independent mechanism and cannabinoid receptor activation apparently does not contribute to EDHF-mediated relaxation in this resistance artery.
内源性大麻素——花生四烯酸乙醇胺，已被认为是一种内皮源性超极化因子（EDHF）。我们发现，花生四烯酸乙醇胺在大鼠肠系膜动脉离体节段诱发的舒张与平滑肌超极化有关。然而，尽管花生四烯酸乙醇胺诱发的舒张被蝎毒素（ChTX）或埃博毒素抑制，但对EDHF诱发舒张的抑制需要ChTX和蜂毒素联合使用。花生四烯酸乙醇胺或EDHF诱发的舒张均未被大麻素受体（CB1）拮抗剂SRI41716A抑制，也未被选择性CB1激动剂模拟。因此，花生四烯酸乙醇胺似乎通过一种不依赖CB1受体的机制引起平滑肌舒张，并且大麻素受体激活显然对该阻力动脉中EDHF介导的舒张没有作用。
