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目的:观察血清素(5-HT)对大鼠心室肌细胞瞬时外向钾电流I_(to)的影响并探讨其作用机制.方法:全细胞膜片箝技术记录I_(to).结果:I_(to)电流密度在正常心肌和肥厚心肌细胞无明显差异.在实验电压为+70mV时,5-HT浓度依赖性抑制I_(to),在正常和肥厚心肌细胞,其半数抑制浓度分别为(4O ±5)μmol/L和(38±7)μmol/L.5-HT_2受体阻断剂米胺舍林和磷脂酶C抑制剂 Compound 48/80均可逆转 5-HT抑制I_(to)的作用;蛋白激酶激动剂醋酸佛波酯显著加强5-HT的抑制作用,而蛋白激酶抑制剂白屈菜季铵碱则逆转5-HT抑制I_(to)的作用.结论:5-HT具有抑制心肌细胞I_(to)的作用.此作用是通过激动 5-HT_2受体,启动磷脂酶C信号转导途径,进一步激活蛋白激酶从而抑制心肌I_(to)。
Objective: To investigate the effect of serotonin (5-HT) on transient outward potassium current (Ito) in rat ventricular myocytes and to explore its mechanism.Methods: Whole-cell patch-clamp technique was used to record Ito.Results: ) Current density in normal myocardium and hypertrophic cardiomyocytes no significant difference in the experimental voltage of +70 mV, 5-HT concentration-dependent inhibition of I_ (to), in normal and hypertrophic cardiomyocytes, the median inhibitory concentrations were (4O ± 5) μmol / L and (38 ± 7) μmol / L of 5-HT 2 receptor blocker, and amine phospholipase C inhibitor 48/80 all reversed the effect of 5-HT on I_ (to) 5-HT was significantly enhanced by the protein kinase agonist phorbol acetate, and that of the protein kinase inhibitor celandine was reversed by 5-HT.Conclusion: 5-HT inhibits cardiomyocytes I_ (to) the role of this role is through the activation of 5-HT_2 receptor, start phospholipase C signal transduction pathway, further activation of protein kinases thereby inhibiting myocardial I_ (to).