| 12297727 |
Shi H, Wang H, Han H, Xu D, Yang B, Nattel S, Wang Z: Ultrarapid delayed rectifier K (+) current in H9c2 rat ventricular cell line: biophysical property and molecular identity. Cell Physiol Biochem. 2002;12(4):215-26.
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). |
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