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Oxime depression of the fast sodium current in myocardial cells
1Department of Pharmacology, University of Yamaguchi, College of Medicine, Ube, Japan.
Abstract:
Effects of diacetyl monoxime on the fast Na+ current were examined by the whole-cell voltage-clamp method in embryonic chick ventricular myocytes. Diacetyl monoxime (10-20 mM) decreased the duration and amplitude of the action potential and depressed the amplitude of the peak fast inward Na+ current by about 25 (10 mM)-45% (20 mM), without affecting other I-V parameters. Neither the activation and inactivation kinetics of the Na+ channels, such as the time to peak current and the time constant of inactivation, nor the steady state characteristics of the inactivation and activation were affected by diacetyl monoxime. It also did not alter the window conductance and the recovery kinetics from inactivation (reactivation). Hence, diacetyl monoxime suppresses the fast Na+ current, without affecting the time-dependent and voltage-dependent kinetics.
Insights
Diacetyl monoxime (DM) reduces the fast sodium current (Na+) in heart cells by decreasing action potential amplitude and duration. However, DM does not alter the timing or voltage-dependent properties of these crucial sodium channels.
Area of Science:
- Cardiovascular Physiology
- Electrophysiology
- Pharmacology
Background:
- The fast sodium current (Na+) is critical for cardiac action potential generation and propagation.
- Understanding modulators of Na+ current is essential for developing antiarrhythmic therapies.
- Diacetyl monoxime (DM) is a chemical compound with potential effects on ion channels.
Purpose of the Study:
- To investigate the effects of diacetyl monoxime on the fast Na+ current in embryonic chick ventricular myocytes.
- To determine if DM alters the amplitude, kinetics, or voltage-dependence of Na+ channels.
Main Methods:
- Whole-cell voltage-clamp technique was employed.
- Embryonic chick ventricular myocytes were used as the experimental model.
- Concentrations of 10-20 mM diacetyl monoxime were applied.
Main Results:
- Diacetyl monoxime (10-20 mM) significantly decreased action potential duration and amplitude.
- The peak amplitude of the fast inward Na+ current was depressed by 25-45%.
- DM did not affect other I-V parameters, activation/inactivation kinetics, steady-state characteristics, window conductance, or recovery kinetics.
Conclusions:
- Diacetyl monoxime selectively suppresses the fast Na+ current in cardiac myocytes.
- The drug's action is independent of the time-dependent and voltage-dependent gating properties of Na+ channels.
- DM's effects suggest a specific interaction with the Na+ current mechanism, distinct from channel kinetics.