Abstract
Voltage gated K+ channels are comprised of a pore-forming α-subunit and one or more accessory subunits and allow for K+ ions to flow along their electrochemical gradient, typically out of the cell, in response to changes in membrane potential. Voltage-gated K+ channels act to help set the plateau potential in cardiac cells as well as to repolarize the membrane during an action potential. In cardiac myocytes, they are the primary class of channels responsible for controlling the duration of the action potential, alterations in which can have profound arrhythmic effects. Defects in K+ channel function have been linked to a number of heritable and acquired conditions leading to arrhythmia in affected patients. As we continue to characterize channel function biophysically, our mechanistic understanding of these conditions grows. Hopefully, this will continue to lead to novel therapeutic strategies not only for the relatively rare inherited channelopathies, but more widespread arrhythmias commonly encountered in clinical practice.
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Sampson, K.J., Kass, R.S. (2013). K+ Channelopathies (IKs, IKr, and Ito). In: Gussak, I., Antzelevitch, C. (eds) Electrical Diseases of the Heart. Springer, London. https://doi.org/10.1007/978-1-4471-4881-4_14
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DOI: https://doi.org/10.1007/978-1-4471-4881-4_14
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