Clofilium-induced Block of Delayed Rectifier Type K+Current in Atrial Tumor Cells (AT-1 Cells)
- Resource Type
- Authors
- Mohit Lal Bhattacharyya; Shukla Sarker; Kawonia P Mull; Qadriyyah Debnam
- Source
- Journal of Molecular and Cellular Cardiology. 29:301-307
- Subject
- Genetically modified mouse
Patch-Clamp Techniques
Time Factors
Drug Evaluation, Preclinical
Mice, Transgenic
Tumor cells
Heart Neoplasms
Mice
Lanthanum
Block (telecommunications)
Potassium Channel Blockers
Tumor Cells, Cultured
medicine
Animals
Myocyte
Heart Atria
Reversal potential
Molecular Biology
Chemistry
Clofilium
Mice, Inbred C57BL
Quaternary Ammonium Compounds
Electrophysiology
Delayed rectifier
Mice, Inbred DBA
Biophysics
Female
Cardiology and Cardiovascular Medicine
Anti-Arrhythmia Agents
medicine.drug
- Language
- ISSN
- 0022-2828
Clofilium-induced Block of Delayed Rectifier Type K + Current in Atrial Tumor Cells (AT-1 Cells). Journal of Molecular and Cellular Cardiology (1997) 29 , 301–307. Atrial tumor myocytes derived from transgenic mice (AT-1 cells) have been shown to express mRNAs encoding cardiac K + channels and display a cardiac electrophysiological phenotype. The major K + current is the rapid component of the delayed rectifier (I kr ). The purpose of the study was to characterize the mode of action of a class III anti-arrhythmic agent (C3A), clofilium, in these cells to elucidate further the mechanism and functional consequence of block. We show that clofilium blocks this I kr in a dose-dependent manner with IC 50 of 1.25 μ m . Clofilium induced block was irreversible for higher concentrations (≥50 μ m ) and partially reversible for lower doses. The reversal potential for this current was −77.5±1.5 mV. The block is voltage dependent and the drug probably binds the channel in the open state.