目的 分析6，7-二甲氧基香豆素(DMOC)对α₁受体、H₁受体、M₃受体和钙通道的影响。方法 以去甲肾上腺素(NE)、组胺、高钾和苯肾上腺素引起兔主动脉条收缩；用阿托品协同NE引起离体灌流肾灌注压升高。结果 DMOC使NE和组胺引起动脉条收缩的量效曲线平行右移，但在高剂量时收缩不能达最大值；不拮抗高钾引起的收缩，而拮抗苯肾上素引起无钙液中的动脉条收缩；阿托品对DMOC拮抗NE引起灌流肾灌注压的升高并无影响。结论 DMOC为α₁受体和H₁受体的竞争性拮抗剂，且抑制内钙释放，但对电压门控钙通道和M₃受体无作用。

OBJECTIVE To investigate the role of 6,7-dimethoxycoumarin (DMOC) on α1-R,H1-R,M3-R and calcium channel.METHODS NE,histamine,KCl and phenylephedrinum were used to induce the contraction of the rabbit aortic strip.Atropine was added when NE was used to increase the perfusion pressure.RESULTS DMOC parallelly moved the dose-effect curve of histamine or NE,but the contraction could not reach the maximum at the large amount.It did not suppress the contraction to KCl,while reversed that to phenylephedrinum in Ca2+free Krebs solution.The effect of DMOC on the dose-effect curve of NE was not influenced by atropine on the isolated perfused kidney.CONCLUSION DMOC was the antagonist both for α1-R and H1-R and inhibited the release of Ca2+from sarcoplasmic reticulum.However,it did not have effect on voltage dependent Ca2+channel and M-3-R.