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Decreases of voltage-dependent K^+ currents densities in ventricular myocytes of guinea pigs by chronic oxidant stress
引用本文:Dong DL,Liu Y,Zhou YH,Song WH,Wang H,Yang BF. Decreases of voltage-dependent K^+ currents densities in ventricular myocytes of guinea pigs by chronic oxidant stress[J]. Acta pharmacologica Sinica, 2004, 25(6): 751-755
作者姓名:Dong DL  Liu Y  Zhou YH  Song WH  Wang H  Yang BF
作者单位:De-li DONG,Yan LIU,Yu-hong ZHOU,Wei-hua SONG,He WANG,Bao-feng YANG2 Department ofpharmacology,Harbin Medical University,Harbin 150086,China
基金项目:Project supported by the Natural Science Foundation ofHeilongjiang Province (No D0246)and the NationalNatural Sci-ence Foundation of China (No 30271599).
摘    要:INTRODUCTION Intracellular K concentration plays an importantrole in the regulation of apoptosis process[1]. ExcessiveK efflux and intracellular K depletion may be respon-sible for the cell shrinkage and apoptotic death[2,3]. Cel-lular K homeostasis is maintained by K efflux and K uptake mechanism. Voltage-dependent K currents arethe major pathways for the K efflux, which indicatesthat voltage-dependent K currents are involved in theapoptosis. Several studies reported th…

关 键 词:电压依赖K^+通路  密度减少  心室肌细胞  慢性氧化剂作用  豚鼠  原发性心肌病

Decreases of voltage-dependent K+ currents densities in ventricular myocytes of guinea pigs by chronic oxidant stress
Dong De-Li,Liu Yan,Zhou Yu-Hong,Song Wei-Hua,Wang He,Yang Bao-Feng. Decreases of voltage-dependent K+ currents densities in ventricular myocytes of guinea pigs by chronic oxidant stress[J]. Acta pharmacologica Sinica, 2004, 25(6): 751-755
Authors:Dong De-Li  Liu Yan  Zhou Yu-Hong  Song Wei-Hua  Wang He  Yang Bao-Feng
Affiliation:Department of pharmacology, Harbin Medical University, Harbin 150086, China.
Abstract:AIM: To determine the changes of delayed rectifier K(+) currents (I(k)) and inward rectifier K(+) currents (I(k1)) in the ventricular myocytes of guinea pigs during the gradual apoptotic process by the chronic oxidant stress treatment. METHODS: H(2)O(2) 50 micromol/L (24 h) was used for inducing apoptosis in the cardiomyocytes culture of neonatal rats and to treat the isolated ventricular myocytes of adult guinea pigs in vitro for 24 h. Apoptosis was evaluated by TUNEL methods and voltage-dependent K(+) currents were recorded by patch-clamp techniques. RESULTS: H(2)O(2) 50 micromol/L (24 h) induced cell apoptosis in the cardiomyocytes culture of neonatal rats. This concentration was used to treat the isolated ventricular myocytes of adult guinea pigs in vitro for 24 h and the voltage-dependent K(+) currents densities (I(k), I(k1)) were down-regulated. The densities of the delayed rectifier K(+) currents (I(k)) in 50 micromol/L H(2)O(2) group were 2.52+/-0.57 pA/pF vs 5.73+/-1.84 pA/pF in the control group at +50 mV (n=8, P<0.01). The densities of the inward rectifier K(+) currents (I(k1)) in 50 micromol/L H(2)O(2) group were -13.9+/-2.70 pA/pF, 2.52+/-0.57 pA/pF vs -59.7+/-11.9 pA/pF, 5.73+/-1.84 pA/pF in the control group at -120 mV (n=8, P<0.01) and -40 mV (n=8, P<0.05), respectively. The extent of inward rectifier property of I(k1) was weakened by 50 micromol/L H(2)O(2) treatment. CONCLUSION: The densities of I(k), I(k1) in the cardiomyocytes of guinea pigs were down-regulated and the inward rectifier property of I(k1) was weakened during the gradual apoptotic process after 50 micromol/L H(2)O(2) treatment for 24 h.
Keywords:hydrogen peroxide  potassium  apoptosis  cardiac myocytes
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