科研之友
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摘要
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-PKC 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-staining of the cytoplasmic membrane of H9c2 cells was seen only with Kv3.1b antibody. Antisense oligodeoxynucleoticles 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.
