title: Properties and functions of KATP during mouse perinatal development.
abstract: BACKGROUND
  Prevailing data suggest that ATP-sensitive potassium channels (K(ATP)) contribute to a surprising resistance to hypoxia in mammalian embryos, thus we aimed to characterize the developmental changes of K(ATP) channels in murine fetal ventricular cardiomyocytes.
  
  
  METHODS
  Patch clamp was applied to investigate the functions of K(ATP). RT-PCR, Western blot were used to further characterize the molecular properties of K(ATP) channels.
  
  
  RESULTS
  Similar K(ATP) current density was detected in ventricular cardiomyocytes of late development stage (LDS) and early development stage (EDS). Molecular-biological study revealed the upregulation of Kir6.1/SUR2A in membrane and Kir6.2 remained constant during development. Kir6.1, Kir6.2, and SUR1 were detectable in the mitochondria without marked difference between EDS and LDS. Acute hypoxia-ischemia led to cessation of APs in 62.5% of tested EDS cells and no APs cessation was observed in LDS cells. SarcK(ATP) blocker glibenclamide rescued 47% of EDS cells but converted 42.8% of LDS cells to APs cessations under hypoxia-ischemic condition. MitoK(ATP) blocker 5-HD did not significantly influence the response to acute hypoxia-ischemia at either EDS or LDS. In summary, sarcK(ATP) played distinct functional roles under acute hypoxia-ischemic condition in EDS and LDS fetal ventricular cardiomyocytes, with developmental changes in sarcK(ATP) subunits. MitoK(ATP) were not significantly involved in the response of fetal cardiomyocytes to acute hypoxia-ischemia and no developmental changes of K(ATP) subunits were found in mitochondria.
authors.affiliation: Department of Physiology, Tongji Medical College, Huazhong University of Science and Technology, Hangkong Road 13, Wuhan 430030, China.
authors.forename: Li
authors.initials: L
authors.lastname: Nie
authors.forename: Ming
authors.initials: M
authors.lastname: Tang
authors.forename: Ying
authors.initials: Y
authors.lastname: Zeng
authors.forename: Huaping
authors.initials: H
authors.lastname: Jiang
authors.forename: Hangchuan
authors.initials: H
authors.lastname: Shi
authors.forename: Hongyan
authors.initials: H
authors.lastname: Luo
authors.forename: Xinwu
authors.initials: X
authors.lastname: Hu
authors.forename: Linlin
authors.initials: L
authors.lastname: Gao
authors.forename: Jiaoya
authors.initials: J
authors.lastname: Xi
authors.forename: Aifen
authors.initials: A
authors.lastname: Liu
authors.forename: Michael
authors.initials: M
authors.lastname: Reppel
authors.forename: Jürgen
authors.initials: J
authors.lastname: Hescheler
authors.forename: Huamin
authors.initials: H
authors.lastname: Liang
mesh_terms: D018528:ATP-Binding Cassette Transporters / Q000819:agonists / Q000235:genetics / Q000378:metabolism; D000818:Animals; D015687:Cell Hypoxia; D006352:Heart Ventricles / Q000196:embryology* / Q000378:metabolism; D054086:KATP Channels / Q000819:agonists / Q000235:genetics / Q000378:metabolism; D049990:Membrane Transport Modulators / Q000494:pharmacology; D051379:Mice; D008815:Mice, Inbred Strains; D008929:Mitochondria, Heart / Q000378:metabolism*; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000502:physiology*; D020110:Pinacidil / Q000494:pharmacology; D015221:Potassium Channels / Q000819:agonists / Q000235:genetics / Q000378:metabolism*; D024661:Potassium Channels, Inwardly Rectifying / Q000819:agonists / Q000235:genetics / Q000378:metabolism; D011955:Receptors, Drug / Q000819:agonists / Q000235:genetics / Q000378:metabolism; D064233:Sulfonylurea Receptors; D000099161:Kcnj11 Channel
chemical_list: D018528:ATP-Binding Cassette Transporters; D054086:KATP Channels; D049990:Membrane Transport Modulators; D020110:Pinacidil; D015221:Potassium Channels; D024661:Potassium Channels, Inwardly Rectifying; D011955:Receptors, Drug; D064233:Sulfonylurea Receptors; D000099161:Kcnj11 Channel; C577508:Abcc8 protein, mouse; C577511:Abcc9 protein, mouse; C117780:mitochondrial K(ATP) channel; C092520:uK-ATP-1 potassium channel