A1腺苷受体在吡那地尔预处理诱导失血性休克大鼠血管反应性保护中的作用

摘要

目的 观察吡那地尔预处理是否通过腺苷受体诱导蛋白激酶Cα(PKCα)、蛋白激酶Cε(PKCε)活化和失血性休克血管反应性和钙敏感性保护.方法 观察吡那地尔预处理后腺苷浓度变化,A1、A2A、A2B、A3腺苷受体(A1R、A2AR、A2BR和A3R)抑制剂对吡那地尔预处理诱导PKCα和PKCε转位、以及血管反应性和钙敏感性保护的影响.结果吡那地尔休克前30 min预处理可使休克2 h腺苷浓度由7.299mg/L增高至11.626 mg/L(P<0.01).吡那地尔预处理可诱导PKCα和PKCε转位、失血性休克血管反应性和钙敏感性保护,A1R拮抗剂可抑制上述效应(P<0.01).结论 吡那地尔预处理通过A1R,诱导PKCα和PKCε活化和失血性休克血管反应性和钙敏感性保护.%Objective To observe the role of adenosine receptor in the pinacidil pretreatment-induced activation of protein kinase Cα ( PKCα),protein kinase Ce (PKCε) and protection of vascular reactivity and calcium sensitivity after hemorrhagic shock in rats.Methods The changes of adenosine concentration after pinacidil pretreatment,the effects of A1,A2A,A2B and A3 adenosine receptors (A1 R,A2A R,A2BR and A3 R) inhibitors on the pinacidil pretreatment-induced protein expression and translocation of PKCα and PKCε,and the effects of A1R,A2AR,A2BR and A3R inhibitors on the pinacidil pretreatmentinduced protection of vascular reactivity and calcium sensitivity after hemorrhagic shock were measured.Results Pinacidil pretreatment implemented at 30 min before shock could increase the adenosine concentration at 2 h after shock from 7.299 to 11.626 mg/L ( P ＜ 0.01 ); Pinacidil pretreatment could promote the translocation of PKCα and PKCε from cytoplasm to membrane (P ＜0.01 ),and induce the protection of vascular reactivity and calcium sensitivity after hemorrhagic shock,which were all inhibited by A1 R inhibitor ( P ＜ 0.01 ).Conclusion Pinacidil pretreatment could induce the activation of PKCα,PKCε and the protection of vascular reactivity and calcium sensitivity after hemorrhagic shock in rats through A1 R.