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首页> 外文期刊>Life sciences >ACTIVATION OF PROTEIN KINASE A PARTIALLY REVERSES THE EFFECTS OF 2,3-BUTANEDIONE MONOXIME ON THE TRANSIENT OUTWARD K+ CURRENT OF RAT VENTRICULAR MYOCYTES
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ACTIVATION OF PROTEIN KINASE A PARTIALLY REVERSES THE EFFECTS OF 2,3-BUTANEDIONE MONOXIME ON THE TRANSIENT OUTWARD K+ CURRENT OF RAT VENTRICULAR MYOCYTES

机译：蛋白质激酶A的激活部分逆转了2,3-丁二酮单肟对大鼠心室肌细胞瞬时向外K +电流的影响

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The transient outward K+ current (I-to) was assessed in single rat ventricular myocytes with the whole-cell patch-clamp technique. Extracellular application of the chemical phosphatase 2,3-butanedione monoxime (BDM) inhibited I-to in a concentration-dependent manner. The IC50 was 14 mM. The on-set of this effect occurred within 20 s after BDM application. I-to recovered almost completely at 2 min after washout of BDM. Application of 20 mM BDM shifted the steady-state inactivation curve of I-to by 9 +/- 2 mV (n = 8) in the negative direction. Addition of 5 mu M isoproterenol enhanced I-to amplitude by 16.2 +/- 1.8%. This concentration of isoproterenol partially reversed the BDM-induced inhibition of I-to+. Furthermore, application of 10 mM 8-bromoadenosine 3':5'-cyclic monophosphate enhanced the amplitude of I-to and also significantly reversed the BDM-induced suppression of I-to. In contrast, intracellular dialysis with guanosine 3':5'-cyclic monophosphate (cGMP, 1-10 mM) did not affect the BDM-induced inhibition of I-to. The inward rectifier K+ current (I-k1) was relatively insensitive to BDM; i.e., 20 mM BDM inhibited I-to and I-k1 to 35.5 +/- 4.3% (n = 8) and 92.9 +/- 4.0% (n = 4) of the control, respectively. These results indicate that BDM suppressed I-to but not I-k1 of rat ventricular myocytes. We attribute the BDM suppression of I-to to dephosphorylation of the channel protein. [References: 36]
机译：使用全细胞膜片钳技术评估单个大鼠心室肌细胞的瞬时向外K +电流（I-to）。在细胞外应用化学磷酸酶2，3-丁二酮单肟（BDM）以浓度依赖的方式抑制I-to。 IC50为14 mM。这种作用的发作发生在BDM应用后20秒之内。冲洗BDM后2分钟，I-几乎完全恢复。 20 mM BDM的施加使I-to的稳态灭活曲线在负方向上移动了9 +/- 2 mV（n = 8）。添加5μM异丙肾上腺素可使I-振幅增加16.2 +/- 1.8％。异丙肾上腺素的这种浓度部分逆转了BDM诱导的I-to +抑制。此外，应用10 mM 8-溴腺苷3'：5'-环一磷酸酯可增强I-to的幅度，并显着逆转BDM诱导的I-to抑制。相反，用鸟苷3'：5'-环一磷酸（cGMP，1-10 mM）进行的细胞内透析不影响BDM诱导的I-to抑制。内向整流器K +电流（I-k1）对BDM相对不敏感;即20 mM BDM分别将I-to和I-k1抑制为对照的35.5 +/- 4.3％（n = 8）和92.9 +/- 4.0％（n = 4）。这些结果表明BDM抑制了大鼠心室肌细胞的I-to而不是I-k1。我们将IDM的BDM抑制归因于通道蛋白的去磷酸化。 [参考：36]

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