PMID- 10432335
OWN - NLM
STAT- MEDLINE
DCOM- 19991018
LR  - 20190513
IS  - 0022-3751 (Print)
IS  - 0022-3751 (Linking)
VI  - 519 Pt 1
DP  - 1999 Aug 15
TI  - Elimination of the transient outward current and action potential prolongation in
      mouse atrial myocytes expressing a dominant negative Kv4 alpha subunit.
PG  - 11-21
AB  - 1. Analyses of whole-cell voltage-clamp recordings from isolated adult (C57BL6)
      mouse atrial myocytes reveal the presence of two prominent Ca2+-independent
      depolarization-activated K+ currents: a rapidly activating and inactivating,
      transient outward K+ current, Ito,f; and a non-inactivating, steady-state, K+
      current, Iss. 2. The properties of Ito,f and Iss in adult mouse atrial myocytes
      are similar to those of the analogous currents recently described in detail in
      adult mouse ventricular cells. A slowly inactivating K+ current, which is similar
      to IK,slow in ventricular cells, is detected in approximately 40 % of adult mouse
      atrial myocytes, and when expressed, the density of this current component is
      substantially lower than the density of Ito,f or Iss. 3. The similarity between
      atrial and ventricular Ito,f and the finding that both the Kv4 subfamily alpha
      subunits, Kv4.2 and Kv4.3, are expressed in wild-type mouse atria prompted us to 
      determine if atrial Ito,f is affected in transgenic mice expressing a mutant Kv4.
      2 alpha subunit, Kv4.2W362F, that functions as a dominant negative. 4. Similar to
      findings in ventricular cells, electrophysiological recordings reveal that Ito,f 
      is selectively eliminated in atrial myocytes isolated from transgenic mice
      expressing Kv4.2W362F, thereby demonstrating directly that Kv4 subfamily members 
      also underlie mouse atrial Ito,f. 5. Neither the steady-state, non-inactivating
      K+ current Iss, nor the inwardly rectifying K+ current IK1, in atrial myocytes is
      affected by the expression of Kv4. 2W362F.6 In contrast to previous findings in
      Kv4.2W362F-expressing mouse ventricular myocytes, there is no evidence that
      electrical remodelling occurs in atrial cells when Ito,f is functionally
      eliminated. 6. The elimination of Ito,f is accompanied by marked increases in
      atrial action potential durations, although no electrocardiographic abnormalities
      attributable to, or suggestive of, altered atrial functioning are evident in
      Kv4.2W362F-expressing animals.
FAU - Xu, H
AU  - Xu H
AD  - Department of Molecular Biology and Pharmacology, Washington University Medical
      School, St Louis, MO 63110, USA.
FAU - Li, H
AU  - Li H
FAU - Nerbonne, J M
AU  - Nerbonne JM
LA  - eng
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - J Physiol
JT  - The Journal of physiology
JID - 0266262
RN  - 0 (KCND2 protein, human)
RN  - 0 (KCND3 protein, human)
RN  - 0 (Kcnd2 protein, mouse)
RN  - 0 (Kcnd3 protein, mouse)
RN  - 0 (Macromolecular Substances)
RN  - 0 (Potassium Channels)
RN  - 0 (Potassium Channels, Voltage-Gated)
RN  - 0 (Shal Potassium Channels)
RN  - 12629-01-5 (Human Growth Hormone)
RN  - EC 3.6.4.1 (Myosin Heavy Chains)
SB  - IM
MH  - Action Potentials/*physiology
MH  - Animals
MH  - Cells, Cultured
MH  - Heart/*physiology
MH  - Heart Atria
MH  - Heart Ventricles
MH  - Human Growth Hormone/genetics
MH  - Humans
MH  - Macromolecular Substances
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Transgenic
MH  - Myocardium/cytology
MH  - Myosin Heavy Chains/genetics
MH  - Patch-Clamp Techniques
MH  - Potassium Channels/chemistry/genetics/*physiology
MH  - *Potassium Channels, Voltage-Gated
MH  - Promoter Regions, Genetic
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Shal Potassium Channels
PMC - PMC2269475
EDAT- 1999/08/05 00:00
MHDA- 1999/08/05 00:01
CRDT- 1999/08/05 00:00
PHST- 1999/08/05 00:00 [pubmed]
PHST- 1999/08/05 00:01 [medline]
PHST- 1999/08/05 00:00 [entrez]
AID - PHY_9166 [pii]
AID - 10.1111/j.1469-7793.1999.0011o.x [doi]
PST - ppublish
SO  - J Physiol. 1999 Aug 15;519 Pt 1:11-21. doi: 10.1111/j.1469-7793.1999.0011o.x.