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目的:研究牛磺酸(Tau)对血管的舒张作用并探讨其机制。方法:采用大鼠离体主动脉环灌流模型,经生物信号采集与分析系统测定Tau 10,20,40,80 mmol.L-1对苯肾上腺素(PE)1μmol.L-1和氯化钾(KCl)60 mmol.L-1预收缩内皮完整和去内皮血管的舒张作用,及Tau对不同工具药血管反应性的影响。结果:Tau能非血管内皮依赖性舒张由PE和KCl诱导收缩的大鼠胸主动脉环;对PE诱发的依赖内钙释放和外钙内流的血管环收缩均有抑制作用;对咖啡因诱导的血管环收缩无明显抑制作用;格列苯脲和四乙胺能够明显抑制Tau的舒张血管作用,但氯化钡和4-氨基吡啶不能抑制其舒张血管作用。结论:Tau的血管舒张作用是非内皮依赖性的,其机制可能是通过抑制血管平滑肌依内Ca2+性收缩(IP3介导)和依外Ca2+性收缩起作用的。同时KATP通道和KCa通道可能参与了Tau的舒血管作用。
Objective: To study the vasorelaxant effect of taurine (Tau) and explore its mechanism. METHODS: Rat isolated aortic ring perfusion model was used to determine Tau 10,20,40,80 mmol.L-1 phenylephrine (PE) 1 μmol.L-1 and potassium chloride by a biological signal acquisition and analysis system. (KCl) 60 mmol.L-1 Precontraction Endothelial Integrity and Endothelial Vascular Relaxation, and Effects of Tau on Vascular Reactivity of Different Tools. Results: Tau non-vascular endothelium-dependent relaxation induced contraction of rat thoracic aorta rings by PE and KCl; inhibition of PE-induced intra-calcium release and extracellular calcium influx in vascular ring contraction; and caffeine induction The vasoconstriction of the vascular rings had no obvious inhibitory effect; glibenclamide and tetraethylamine could significantly inhibit the vasodilating effect of Tau, but cesium chloride and 4-aminopyridine could not inhibit the vasodilatory effects. CONCLUSIONS: The vasodilating effect of Tau is non-endothelial-dependent, and its mechanism may be through the inhibition of intravascular Ca 2+ -induced contraction (IP3-mediated) and extracellular Ca 2+ -induced contraction of vascular smooth muscle. At the same time, KATP and KCa channels may be involved in the vasodilatory effects of Tau.