Compared to the expression of potassium channels Kv9.1, Kv9.2, Kv9.3 mRNA on the 7 day after myocardial infarction, potassium channels Kv9.1, Kv9.2, Kv9.3 mRNA remarkably decreased on the 30 day (P<0.05).
②Different kinds of potassium channel blockers, such as 1 mmol/L tetraethylammonium, 1 mmol/L 4-aminopyridine, 100 nmol/L Iberiotoxin(IBTX) or 100 μmol/L paxilline were added into culture medium ten minutes before the treatment of SNP (0.1 mmol/L) and neuronal survival rate were estimated 18 hours later.
The animals received isoflurane(1.2%~1.5%) preconditioning 60 minutes before I/R in ISO group,received 5-HD(10 mg/kg),the mitochondrial ATP-sensitive K+ channel(mitoKATP) blocker,and ISO before I/R in 5-HD+ISO group,and received 5-HD 30 minutes before I/R in 5-HD group.
The results showed that ①In whole cell recordings with voltage ramp protocol,a Voltage dependent K +(Kv) channels was recorded in Daudi cells,which was sensitive to quinine 100 μmol·L -1 and charybdotoxin (CTX) 100 nmol·L -1 ,K + channel blockers.
Results: A big conductance calcium activated K + channel was observed,with symmetrical 140mol/L across patches,in ward conductance was (171±12) pS and change little as different [Ca 2+ ] was included in the bath solution. Outward conductance was regulated by and was (76±14)pS with 500 μmol/L [Ca 2+ ].
The HeLa cells were prevented partially from As_2O_3-induced cell death by co-application for 24h with typical voltage- dependent K~+ channel blockers,4-aminopyridine (3mmol·L~(-1)) or tetraethylammonium (5mmol· L~(-1)).
As_2O_3诱导的 HeLa 细胞死亡可被共同孵育钾通道阻滞剂四氨基吡啶(3mmol·L~(-1))或四乙基铵(5mmol·L~(-1))所部分抑制。
Conclusion Chronic treatment with As_2O_3 increased voltage-dependent K~+ currents in HeLa cells and the cell death induced by As_2O_3 was reduced partially by voltage-dependent K~+ channel blockers,4-aminopyridine or tetraethylammonium.
结论 As_2O_3长期处理增加 HeLa 细胞的电压依赖性钾电流。 As_2O_3诱导的 HeLa 细胞死亡可被钾通道阻滞剂四氨基吡啶或四乙基铵部分抑制。
Objective To investigate the effect of voltage dependent K~+ channel blocker(4-aminopyridine,4-AP) and calcium activated K~+ channel blocker(tetraethylammonia,TEA)on human pulmonary adenocarcinoma AGZY-83-a cell line and to explore its mechanism.
Role of Opiate Receptors and ATP-Dependent Potassium Channels of Mitochondria in the Formation of Myocardial Adaptive Resistance
The Role of Potassium, Potassium Channels, and Symporters in the Apoptotic Cell Volume Decrease: Experiment and Theory
Potential RNase targets in a tumor cell and the role of modulation of calcium-dependent potassium channels and the ras oncogene in RNase-induced cell damage are considered.
The conductance of outward- and inward-rectifying potassium channels, as well as the currents of excitable chloride channels, decreased after 2-3 days of heat treatment.
By the 15th-17th days, the conductance of potassium channels was reduced by a factor of 3-5, whereas the peak values of the chloride current, associated with the action potential, was reduced by a factor of 8-10.