title: Decreases of voltage-dependent K+ currents densities in ventricular myocytes of guinea pigs by chronic oxidant stress.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of pharmacology, Harbin Medical University, Harbin 150086, China.
authors.forename: De-Li
authors.initials: DL
authors.lastname: Dong
authors.forename: Yan
authors.initials: Y
authors.lastname: Liu
authors.forename: Yu-Hong
authors.initials: YH
authors.lastname: Zhou
authors.forename: Wei-Hua
authors.initials: WH
authors.lastname: Song
authors.forename: He
authors.initials: H
authors.lastname: Wang
authors.forename: Bao-Feng
authors.initials: BF
authors.lastname: Yang
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis / Q000187:drug effects*; D002478:Cells, Cultured; D015536:Down-Regulation; D006168:Guinea Pigs; D006352:Heart Ventricles / Q000166:cytology; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D032383:Myocytes, Cardiac / Q000187:drug effects* / Q000502:physiology; D018384:Oxidative Stress / Q000187:drug effects*; D018408:Patch-Clamp Techniques; D015221:Potassium Channels / Q000187:drug effects; D024661:Potassium Channels, Inwardly Rectifying / Q000187:drug effects*; D051381:Rats; D017208:Rats, Wistar
chemical_list: D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying; D006861:Hydrogen Peroxide