Using patch clamp whole cell recording techiques, we examined the effects ofIQ_23, a benzyl-isoquinoline derivative with antiarrhythmic activities, on the action potential (AP) andpotassium currents in single guinea p...Using patch clamp whole cell recording techiques, we examined the effects ofIQ_23, a benzyl-isoquinoline derivative with antiarrhythmic activities, on the action potential (AP) andpotassium currents in single guinea pig ventricular myocytes. The results showed that IQ_23 at 10, 30and 100 μmol ·L_-1 slowed the repolarization in AP dose-dependently. The APD_90 were prolonged by15%, 28% and 31% respectively. This effect did not depend on the extracellular Ca^2+. In voltageclamp mode, IQ_23 effectively blocked both the components of the delayed rectifier potassium current(I_k), i.e., I_ks and I_kr. At concentrations of 30 and 100 μmol· L^-1, IQ_23 suppressed I_ks by 21% and 26%and suppressed I_kr by 67% and 86% respectively. But even at 100 μmol·L^-1, IQ_23 had little effect onthe inward rectifier potassium current (I_k1). It is concluded: 1. IQ_23 can dose-dependently prolongAPD in the ventriculas myocytes of guinea pig, the effect does not depend on the extracellular Ca^2+; 2.IQ_23 blocks both I_ks and Ikr in the ventricular myocytes without obvious specificities between them.展开更多
Using patch clamp whole cell recording techiques, we examined the effects ofIQ<sub>2</sub>3, a benzyl-isoquinoline derivative with antiarrhythmic activities, on the action potential （AP） andpotassium cur...Using patch clamp whole cell recording techiques, we examined the effects ofIQ<sub>2</sub>3, a benzyl-isoquinoline derivative with antiarrhythmic activities, on the action potential （AP） andpotassium currents in single guinea pig ventricular myocytes. The results showed that IQ<sub>2</sub>3 at 10, 30and 100 μmol ·L<sub>-</sub>1 slowed the repolarization in AP dose-dependently. The APD<sub>9</sub>0 were prolonged by15%, 28% and 31% respectively. This effect did not depend on the extracellular Ca<sup>2</sup>+. In voltageclamp mode, IQ<sub>2</sub>3 effectively blocked both the components of the delayed rectifier potassium current（I<sub>k</sub>）, i.e., I<sub>k</sub>s and I<sub>k</sub>r. At concentrations of 30 and 100 μmol· L<sup>-</sup>1, IQ<sub>2</sub>3 suppressed I<sub>k</sub>s by 21% and 26%and suppressed I<sub>k</sub>r by 67% and 86% respectively. But even at 100 μmol·L<sup>-</sup>1, IQ<sub>2</sub>3 had little effect onthe inward rectifier potassium current （I<sub>k</sub>1）. It is concluded: 1. IQ<sub>2</sub>3 can dose-dependently prolongAPD in the ventriculas myocytes of guinea pig, the effect does not depend on the extracellular Ca<sup>2</sup>+; 2.IQ<sub>2</sub>3 blocks both I<sub>k</sub>s and Ikr in the ventricular myocytes without obvious specificities between them.展开更多
目的观察转录因子特异性蛋白1(specific protein 1,Sp1)对心肌细胞Kv2.1钾通道蛋白及电流的影响。方法构建Sp1基因的表达质粒pEGFP-N2-Sp1,转染H9C2心肌细胞。Western blot检测转染前后Kv2.1钾通道蛋白表达,全细胞膜片钳技术检测转染前...目的观察转录因子特异性蛋白1(specific protein 1,Sp1)对心肌细胞Kv2.1钾通道蛋白及电流的影响。方法构建Sp1基因的表达质粒pEGFP-N2-Sp1,转染H9C2心肌细胞。Western blot检测转染前后Kv2.1钾通道蛋白表达,全细胞膜片钳技术检测转染前后Kv2.1电流密度和电流特性的变化。结果与对照组相比,Sp1能明显增强Kv2.1钾通道蛋白表达(P<0.05),增大Kv2.1电流密度(P<0.05)。同时,Sp1减少Kv2.1钾通道的激活时间常数,加快该通道的激活,但半失活最大电压V1/2和斜率因子k值均无明显变化(均P>0.05)。结论Sp1增强Kv2.1钾通道电流,加快该通道的激活。展开更多
文摘Using patch clamp whole cell recording techiques, we examined the effects ofIQ_23, a benzyl-isoquinoline derivative with antiarrhythmic activities, on the action potential (AP) andpotassium currents in single guinea pig ventricular myocytes. The results showed that IQ_23 at 10, 30and 100 μmol ·L_-1 slowed the repolarization in AP dose-dependently. The APD_90 were prolonged by15%, 28% and 31% respectively. This effect did not depend on the extracellular Ca^2+. In voltageclamp mode, IQ_23 effectively blocked both the components of the delayed rectifier potassium current(I_k), i.e., I_ks and I_kr. At concentrations of 30 and 100 μmol· L^-1, IQ_23 suppressed I_ks by 21% and 26%and suppressed I_kr by 67% and 86% respectively. But even at 100 μmol·L^-1, IQ_23 had little effect onthe inward rectifier potassium current (I_k1). It is concluded: 1. IQ_23 can dose-dependently prolongAPD in the ventriculas myocytes of guinea pig, the effect does not depend on the extracellular Ca^2+; 2.IQ_23 blocks both I_ks and Ikr in the ventricular myocytes without obvious specificities between them.
文摘Using patch clamp whole cell recording techiques, we examined the effects ofIQ<sub>2</sub>3, a benzyl-isoquinoline derivative with antiarrhythmic activities, on the action potential （AP） andpotassium currents in single guinea pig ventricular myocytes. The results showed that IQ<sub>2</sub>3 at 10, 30and 100 μmol ·L<sub>-</sub>1 slowed the repolarization in AP dose-dependently. The APD<sub>9</sub>0 were prolonged by15%, 28% and 31% respectively. This effect did not depend on the extracellular Ca<sup>2</sup>+. In voltageclamp mode, IQ<sub>2</sub>3 effectively blocked both the components of the delayed rectifier potassium current（I<sub>k</sub>）, i.e., I<sub>k</sub>s and I<sub>k</sub>r. At concentrations of 30 and 100 μmol· L<sup>-</sup>1, IQ<sub>2</sub>3 suppressed I<sub>k</sub>s by 21% and 26%and suppressed I<sub>k</sub>r by 67% and 86% respectively. But even at 100 μmol·L<sup>-</sup>1, IQ<sub>2</sub>3 had little effect onthe inward rectifier potassium current （I<sub>k</sub>1）. It is concluded: 1. IQ<sub>2</sub>3 can dose-dependently prolongAPD in the ventriculas myocytes of guinea pig, the effect does not depend on the extracellular Ca<sup>2</sup>+; 2.IQ<sub>2</sub>3 blocks both I<sub>k</sub>s and Ikr in the ventricular myocytes without obvious specificities between them.
文摘目的观察转录因子特异性蛋白1(specific protein 1,Sp1)对心肌细胞Kv2.1钾通道蛋白及电流的影响。方法构建Sp1基因的表达质粒pEGFP-N2-Sp1,转染H9C2心肌细胞。Western blot检测转染前后Kv2.1钾通道蛋白表达,全细胞膜片钳技术检测转染前后Kv2.1电流密度和电流特性的变化。结果与对照组相比,Sp1能明显增强Kv2.1钾通道蛋白表达(P<0.05),增大Kv2.1电流密度(P<0.05)。同时,Sp1减少Kv2.1钾通道的激活时间常数,加快该通道的激活,但半失活最大电压V1/2和斜率因子k值均无明显变化(均P>0.05)。结论Sp1增强Kv2.1钾通道电流,加快该通道的激活。
