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Dynamic model for ventricular junctional conductance during the cardiac action potential
Xianming Lin1, Joanna Gemel, Eric C Beyer
1Department of Pharmacology, State University of New York Upstate Medical University, Syracuse, New York 13210, USA.
American Journal of Physiology. Heart and Circulatory Physiology
|October 30, 2004
Summary
Ventricular gap junction conductance (g(j)) significantly decreases during action potentials but recovers rapidly. This voltage-dependent behavior, primarily involving connexin 43, may contribute to arrhythmias.
Area of Science:
- Cardiac Electrophysiology
- Cellular Biology
- Biophysics
Background:
- Gap junctions mediate electrical communication between cardiac cells.
- Their function is crucial for coordinated heartbeats and preventing arrhythmias.
- Understanding connexin protein behavior during action potentials is key.
Purpose of the Study:
- To investigate the voltage and time dependence of junctional conductance (g(j)) in ventricular myocytes.
- To identify the connexin proteins responsible for observed g(j) dynamics.
- To model the behavior of gap junctions during cardiac action potentials.
Main Methods:
- Dual whole-cell patch-clamp recordings on paired neonatal murine ventricular myocytes.
- Application of ventricular action potentials to assess junctional conductance (g(j)).
- Immunohistochemistry and immunoblotting to detect connexin protein expression (Cx43, Cx40, Cx45).
Main Results:
- Junctional conductance (g(j)) decreased by 50% during peak action potential voltages (>100 mV).
- This voltage-dependent inactivation showed time constants that accelerated with increasing transjunctional voltage (V(j)).
- g(j) recovered during repolarization, facilitated during the final 5% of repolarization (<30 mV).
Conclusions:
- Ventricular myocyte gap junctions, primarily composed of connexin 43 (Cx43), exhibit dynamic voltage-dependent inactivation and facilitation.
- A mathematical model accurately predicts g(j) behavior across different stimulation rates.
- These dynamic properties suggest a role for gap junctions in conduction block and triggered arrhythmias during slowed conduction.