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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 analyze the effects of 6, 7 dimethoxycoumarin (DMOC) on α1 receptor, H1 receptor, M3 receptor and calcium channel. METHODS: Norepinephrine (NE), histamine, hyperkalemia, and phenylephrine induced contraction of rabbit aortic strips. The use of atropine in combination with NE caused an increase in renal perfusion pressure in isolated perfused kidneys. RESULTS: The dose-effect curve of DMOC caused NE and histamine-induced arterial strip contraction was shifted to the right, but the contraction could not reach the maximum at high doses; it did not antagonize the hyperkalemia-induced contraction, whereas antagonism to phenylephrine resulted in the absence of calcium in the solution. Arterial bar constriction; atropine has no effect on elevation of perfused renal perfusion pressure by antagonism of NE by DMOC. Conclusions DMOC is a competitive antagonist of α1 and H1 receptors and inhibits intracellular calcium release, but has no effect on voltage-gated calcium channels and M3 receptors.