目的研究四逆汤对高钾和去氧肾上腺素(Phe)收缩大鼠离体主动脉血管环效应的影响。方法观察四逆汤在主动脉环上拮抗KCl(60mmol/L)和Phe(1×10^-9～1×10^-4mmol/L)的收缩血管作用,分别用普萘洛尔(Pro,3×10^-6mmol/L)和BayK8644(BK,1×10^-5mmol/L)干预探讨其机制。结果四逆汤减弱累积浓度的Phe收缩血管的效应,最大值(T_max)减小,Pro不影响四逆汤的拮抗作用;四逆汤减小高钾刺激血管的最大收缩效应,BK不能恢复这种效应。结论四逆汤使Phe的量效曲线右移,并减小其最大效应值,表现为非竞争性拮抗作用;减小高钾收缩血管的作用,Ca²⁺开放剂BK不能恢复四逆汤的抑制作用。四逆汤能阻断α₁受体,其减弱高钾刺激引起的血管收缩可能和钙通道无关。

Object To study the effects of SINI TANG(SNT) on the rat aortic rings pre-contracted by high K⁺ and phenylephrine(Phe).Methods The effects of SNT on the aortic rings in the presence of 60 mmol/L KCl and Phe(1×10^-9-1×10^-4 mmol/L) were observed and their mechanisms were studied after treatment with Propranolol(Pro,3×10^-6 mmol/L) and Bay K8644(BK,1×10^-5 mmol/L) as tool drugs.Results SNT inhibited the contraction induced by cumulative Phe and decreased the maximum tension(T_max);Pro couldn't influence the effects of SNT.SNT attenuated the amplitude of contractile effect of high K⁺;BK couldn't reverse the effects of SNT.Conclusion SNT can shift the dose-response curve to the right and decrease the T_max.It shows that SNT is a kind of noncompetitive antagonism.SNT decreases the effect of high K⁺ against contraction of the artery.BK,a L-type Ca²⁺ channels activator,couldn't recover the inhibition induced by SNT.The results suggest that SNT inhibit α₁ receptor,while calcium channel may not be involved in attenuating the effect of SNT on high K⁺-induced contraction.

北京市自然科学基金项目(7011002)