A Mathematical Model of the Human Cardiac Na+ Channel View Full Text


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Article Info

DATE

2019-02

AUTHORS

Tesfaye Negash Asfaw, Vladimir E. Bondarenko

ABSTRACT

Sodium ion channel is a membrane protein that plays an important role in excitable cells, as it is responsible for the initiation of action potentials. Understanding the electrical characteristics of sodium channels is essential in predicting their behavior under different physiological conditions. We investigated several Markov models for the human cardiac sodium channel NaV1.5 to derive a minimal mathematical model that describes the reported experimental data obtained using major voltage clamp protocols. We obtained simulation results for peak current-voltage relationships, the voltage dependence of normalized ion channel conductance, steady-state inactivation, activation and deactivation kinetics, fast and slow inactivation kinetics, and recovery from inactivation kinetics. Good agreement with the experimental data provides us with the mechanisms of the fast and slow inactivation of the human sodium channel and the coupling of its inactivation states to the closed and open states in the activation pathway. More... »

PAGES

1-27

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/s00232-018-00058-x

DOI

http://dx.doi.org/10.1007/s00232-018-00058-x

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1111409357

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/30637460


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50 schema:description Sodium ion channel is a membrane protein that plays an important role in excitable cells, as it is responsible for the initiation of action potentials. Understanding the electrical characteristics of sodium channels is essential in predicting their behavior under different physiological conditions. We investigated several Markov models for the human cardiac sodium channel Na<sub>V</sub>1.5 to derive a minimal mathematical model that describes the reported experimental data obtained using major voltage clamp protocols. We obtained simulation results for peak current-voltage relationships, the voltage dependence of normalized ion channel conductance, steady-state inactivation, activation and deactivation kinetics, fast and slow inactivation kinetics, and recovery from inactivation kinetics. Good agreement with the experimental data provides us with the mechanisms of the fast and slow inactivation of the human sodium channel and the coupling of its inactivation states to the closed and open states in the activation pathway.
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