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目的观察蛋白激酶A(PKA)及蛋白激酶C(PKC)抑制剂和蛋白脱磷酸化物质对大鼠心室肌细胞ATP敏感性钾电流 (IKATP)的影响 ,探讨克罗卡林 (cromakalim)开放ATP敏感性钾通道的作用机制。方法采用全细胞膜片钳技术记录心室肌细胞IKATP。结果在37℃时克罗卡林 (1μmol·L-1)可阻断ATP的抑制作用 ,诱导出IKATP。PKA抑制剂PKI(6～22)amide (1μmol·L -1),可模拟克罗卡林的作用 ,激活IKATP;而PKC抑制剂calphosticC无此作用。同时还观察到蛋白脱磷酸化物质butanedioemonoxime(BDM,5mmol·L -1)也可诱发出IKATP。结论克罗卡林开放IKATP 机制与抑制PKA的活性有关 ,而与PKC无关。
Objective To investigate the effects of protein kinase A (PKA) and protein kinase C (PKC) inhibitors and protein dephosphorylated substance on ATP-sensitive potassium current (IKATP) in rat ventricular myocytes and to explore the effect of cromakalim on ATP Sensitive potassium channel mechanism of action. Methods Whole-cell patch-clamp technique was used to record IKATP in ventricular myocytes. Results Crotarine (1μmol·L-1) blocked the inhibitory effect of ATP at 37 ℃ and induced IKATP. The PKA (6-22) amide (1μmol·L -1) PKA inhibitor could simulate the effect of clenbuterol and activate IKATP, whereas PKC inhibitor calphosticC did not. It was also observed that the protein dephosphorylation butanedioemonoxime (BDM, 5 mmol·L -1) also induced IKATP. Conclusions The mechanism of opening IKATP by crotaline is related to the inhibition of PKA activity, but not to PKC.