Characterization of chromanol 293B-induced block of the delayed-rectifier K+ current in heart-derived H9c2 cells
| Autor: | Sheng Nan Wu, Yi Ching Lo, Yen Chin Liu, Mei Han Huang, Su Rong Yang |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
Quinidine
Chromanol 293B Heart Ventricles Dendrotoxin Gating Apamin General Biochemistry Genetics and Molecular Biology Cell Line Membrane Potentials chemistry.chemical_compound Potassium Channel Blockers medicine Animals Ventricular Function Myocyte Chromans General Pharmacology Toxicology and Pharmaceutics Sulfonamides Dose-Response Relationship Drug Time constant General Medicine Rats Delayed rectifier chemistry Potassium Channels Voltage-Gated Potassium Biophysics Ion Channel Gating medicine.drug |
| Zdroj: | Life Sciences. 76:2275-2286 |
| ISSN: | 0024-3205 |
| DOI: | 10.1016/j.lfs.2004.09.036 |
| Popis: | The effects of chromanol 293B on ion currents in rat embryonic heart-derived H9c2 cells were investigated in this study. Chromanol 293B suppressed the amplitude of delayed rectified K+ current (I(K)) in a concentration-dependent manner. The IC50 value for chromanol 293B-induced inhibition of I(K) was 8 microM. The I(K) present in these cells, the electrical properties of which resembled those for the Kv2.1-related K+ current, was sensitive to inhibition by quinidine or dendrotoxin, yet not by pandinotoxin-Kalpha, E-4031 or apamin. Chromanol 293B reduced the activation time constant of I(K) and the effective gating charge of this channel. However, little or no modification in the steady-state inactivation of I(K) in response to long-lasting conditioning pulses could be demonstrated in the presence of chromanol 293B. These results clearly demonstrate that chromanol 293B can effectively interact with the K+ channel functionally expressed in H9c2 myoblasts. The chromanol 293B-induced inhibition of these channels could primarily be attributed to open channel block. |
| Databáze: | OpenAIRE |
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