Characterization of chromanol 293B-induced block of the delayed-rectifier K+ current in heart-derived H9c2 cells

Yi Ching Lo, Su Rong Yang, Mei Han Huang, Yen-Chin Liu, Sheng-Nan Wu

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

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 IK was 8 μM. 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-Kα, E-4031 or apamin. Chromanol 293B reduced the activation time constant of IK and the effective gating charge of this channel. However, little or no modification in the steady-state inactivation of IK 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.

Original languageEnglish
Pages (from-to)2275-2286
Number of pages12
JournalLife Sciences
Volume76
Issue number20
DOIs
Publication statusPublished - 2005 Apr 1

Fingerprint

Apamin
Quinidine
Myoblasts
6-cyano-4-(N-ethylsulfonyl-N-methylamino)-3-hydroxy-2,2-dimethylchromane
Inhibitory Concentration 50
Rats
Electric properties
Chemical activation
Ions
E 4031
dendrotoxin

All Science Journal Classification (ASJC) codes

  • Biochemistry, Genetics and Molecular Biology(all)
  • Pharmacology, Toxicology and Pharmaceutics(all)

Cite this

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title = "Characterization of chromanol 293B-induced block of the delayed-rectifier K+ current in heart-derived H9c2 cells",
abstract = "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 IK was 8 μM. 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-Kα, E-4031 or apamin. Chromanol 293B reduced the activation time constant of IK and the effective gating charge of this channel. However, little or no modification in the steady-state inactivation of IK 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.",
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Characterization of chromanol 293B-induced block of the delayed-rectifier K+ current in heart-derived H9c2 cells. / Lo, Yi Ching; Yang, Su Rong; Huang, Mei Han; Liu, Yen-Chin; Wu, Sheng-Nan.

In: Life Sciences, Vol. 76, No. 20, 01.04.2005, p. 2275-2286.

Research output: Contribution to journalArticle

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AU - Yang, Su Rong

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AU - Liu, Yen-Chin

AU - Wu, Sheng-Nan

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N2 - 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 IK was 8 μM. 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-Kα, E-4031 or apamin. Chromanol 293B reduced the activation time constant of IK and the effective gating charge of this channel. However, little or no modification in the steady-state inactivation of IK 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.

AB - 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 IK was 8 μM. 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-Kα, E-4031 or apamin. Chromanol 293B reduced the activation time constant of IK and the effective gating charge of this channel. However, little or no modification in the steady-state inactivation of IK 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.

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