Functional roles of ionic currents in a membrane delimited mouse sino-atrial node model

School Of Mathematical Sciences

Research output: Contribution in Book/Report/Proceedings - With ISBN/ISSN › Conference contribution/Paper › peer-review

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Functional roles of ionic currents in a membrane delimited mouse sino-atrial node model. / Kharche, S.; Higham, J.; Lei, M. et al.
2010 Computing in Cardiology. Vol. 37 IEEE, 2011. p. 421-424 5737999.

Research output: Contribution in Book/Report/Proceedings - With ISBN/ISSN › Conference contribution/Paper › peer-review

Harvard

Kharche, S, Higham, J, Lei, M & Zhang, H 2011, Functional roles of ionic currents in a membrane delimited mouse sino-atrial node model. in 2010 Computing in Cardiology. vol. 37, 5737999, IEEE, pp. 421-424. <https://ieeexplore.ieee.org/document/5737999>

APA

Kharche, S., Higham, J., Lei, M., & Zhang, H. (2011). Functional roles of ionic currents in a membrane delimited mouse sino-atrial node model. In 2010 Computing in Cardiology (Vol. 37, pp. 421-424). Article 5737999 IEEE. https://ieeexplore.ieee.org/document/5737999

Vancouver

Kharche S, Higham J, Lei M, Zhang H. Functional roles of ionic currents in a membrane delimited mouse sino-atrial node model. In 2010 Computing in Cardiology. Vol. 37. IEEE. 2011. p. 421-424. 5737999 Epub 2010 Sept 26.

Author

Kharche, S. ; Higham, J. ; Lei, M. et al. / Functional roles of ionic currents in a membrane delimited mouse sino-atrial node model. 2010 Computing in Cardiology. Vol. 37 IEEE, 2011. pp. 421-424

Bibtex

@inproceedings{90f7eae36e9648fb803222d21a4c655c,

title = "Functional roles of ionic currents in a membrane delimited mouse sino-atrial node model",

abstract = "Functional roles of ionic currents in a membrane delimited sino-atrial node (SAN) cell model were investigated. Ionic currents were blocked and intracellular calcium ([Ca2+]i) buffered to study their effects on action potential (AP) characteristics. The simulations revealed that blocking the hyperpolarization activated current and the T-type calcium current caused an increase of cycle length (CL) due to reduced diastolic depolarization rate (DDR). Blocking of sustained outward (Ist) and sodium currents ( INa,1.1, INa,1.5) had no effect. Blocking the L-type calcium current's Cav1.3 isoform (ICaL1.3) and rapidly activating delayed rectifier arrested pacemaking. Blocking sodiumcalcium exchanger (I NaCa) caused a CL reduction but did not affect DDR. Reducing [Ca 2+]i increased CL marginally. A small increase of [Ca 2+]i arrestedpacemaking. Ist, I Na1.1, and INa1.5are not functional and INaCa is a background current in the model.",

author = "S. Kharche and J. Higham and M. Lei and H. Zhang",

year = "2011",

month = mar,

day = "22",

language = "English",

volume = "37",

pages = "421--424",

booktitle = "2010 Computing in Cardiology",

publisher = "IEEE",

}

RIS

TY - GEN

T1 - Functional roles of ionic currents in a membrane delimited mouse sino-atrial node model

AU - Kharche, S.

AU - Higham, J.

AU - Lei, M.

AU - Zhang, H.

PY - 2011/3/22

Y1 - 2011/3/22

N2 - Functional roles of ionic currents in a membrane delimited sino-atrial node (SAN) cell model were investigated. Ionic currents were blocked and intracellular calcium ([Ca2+]i) buffered to study their effects on action potential (AP) characteristics. The simulations revealed that blocking the hyperpolarization activated current and the T-type calcium current caused an increase of cycle length (CL) due to reduced diastolic depolarization rate (DDR). Blocking of sustained outward (Ist) and sodium currents ( INa,1.1, INa,1.5) had no effect. Blocking the L-type calcium current's Cav1.3 isoform (ICaL1.3) and rapidly activating delayed rectifier arrested pacemaking. Blocking sodiumcalcium exchanger (I NaCa) caused a CL reduction but did not affect DDR. Reducing [Ca 2+]i increased CL marginally. A small increase of [Ca 2+]i arrestedpacemaking. Ist, I Na1.1, and INa1.5are not functional and INaCa is a background current in the model.

AB - Functional roles of ionic currents in a membrane delimited sino-atrial node (SAN) cell model were investigated. Ionic currents were blocked and intracellular calcium ([Ca2+]i) buffered to study their effects on action potential (AP) characteristics. The simulations revealed that blocking the hyperpolarization activated current and the T-type calcium current caused an increase of cycle length (CL) due to reduced diastolic depolarization rate (DDR). Blocking of sustained outward (Ist) and sodium currents ( INa,1.1, INa,1.5) had no effect. Blocking the L-type calcium current's Cav1.3 isoform (ICaL1.3) and rapidly activating delayed rectifier arrested pacemaking. Blocking sodiumcalcium exchanger (I NaCa) caused a CL reduction but did not affect DDR. Reducing [Ca 2+]i increased CL marginally. A small increase of [Ca 2+]i arrestedpacemaking. Ist, I Na1.1, and INa1.5are not functional and INaCa is a background current in the model.

M3 - Conference contribution/Paper

VL - 37

SP - 421

EP - 424

BT - 2010 Computing in Cardiology

PB - IEEE

ER -

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