title: Ultrarapid delayed rectifier K(+) current in H9c2 rat ventricular cell line: biophysical property and molecular identity.
abstract: Ultrarapid delayed rectifier K(+) currents (I(Kur)s) contribute importantly to cardiac repolarization. However, understanding of I(Kur)s has been hampered by the difficulty of dissecting them from overlapping currents in primary cells. We found with whole-cell patch-clamp recordings that H9c2 cells, a rat ventricular cell line, under 50% confluence (single myoblasts) express exclusively I(Kur)-like current which activates rapidly upon depolarization and partially inactivates during 150-ms pulses. The H9c2 I(Kur) activates within the same voltage range as native cardiac I(Kur)s, with a half-activation voltage of -13 mV. The H9c2 I(Kur) can be completely blocked by tetraethylammonium and 4-aminopyridine. Reversal potential (-79 mV) and envelope-of tail analyses indicate that the H9c2 I(Kur) is carried by a single population of K(+) channels. H9c2 I(Kur) was increased by beta-adrenoceptor-PKA and decreased by alpha(1)-adrenoceptor-PKC activation by isoproterenol and phenylephrine, respectively. Immunocytochemistry was performed with antibodies against 11 different K(+) channels. Positive immuno-stain-ing of the cytoplasmic membrane of H9c2 cells was seen only with Kv3.1b antibody. Antisense oligodeoxynucleotides directed against Kv3.1b subunit sequence significantly inhibited the H9c2 I(Kur). We conclude that the H9c2 cells at the myoblast stage express mainly I(Kur) and Kv3.1b may be a molecular component of the H9c2 I(Kur), and H9c2 cells provide a suitable system for studying I(Kur).
authors.affiliation: Research Center, Montreal Heart Institute, Montreal, Canada.
authors.forename: Hong
authors.initials: H
authors.lastname: Shi
authors.forename: Huizhen
authors.initials: H
authors.lastname: Wang
authors.forename: Hong
authors.initials: H
authors.lastname: Han
authors.forename: Donghui
authors.initials: D
authors.lastname: Xu
authors.forename: Baofeng
authors.initials: B
authors.lastname: Yang
authors.forename: Stanley
authors.initials: S
authors.lastname: Nattel
authors.forename: Zhiguo
authors.initials: Z
authors.lastname: Wang
mesh_terms: D015761:4-Aminopyridine / Q000494:pharmacology; D000316:Adrenergic alpha-Agonists / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D002460:Cell Line; D006352:Heart Ventricles / Q000166:cytology / Q000378:metabolism*; D007545:Isoproterenol / Q000494:pharmacology; D007700:Kinetics; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D018485:Muscle Fibers, Skeletal / Q000378:metabolism; D032446:Myoblasts / Q000378:metabolism; D009479:Neuropeptides / Q000378:metabolism; D016376:Oligonucleotides, Antisense / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D010656:Phenylephrine / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism* / Q000502:physiology; D026902:Potassium Channel Blockers / Q000494:pharmacology; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism*; D024642:Potassium Channels, Voltage-Gated; D051381:Rats; D051670:Shaw Potassium Channels; D019789:Tetraethylammonium / Q000494:pharmacology
chemical_list: D000316:Adrenergic alpha-Agonists; D000318:Adrenergic beta-Agonists; D009479:Neuropeptides; D016376:Oligonucleotides, Antisense; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D024642:Potassium Channels, Voltage-Gated; D051670:Shaw Potassium Channels; D010656:Phenylephrine; D019789:Tetraethylammonium; D015761:4-Aminopyridine; D007545:Isoproterenol; D011188:Potassium