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Action Potential Duration, Rate of Stimulation, and Intracellular Sodium
Author(s) -
CARMELIET EDWARD
Publication year - 2006
Publication title -
journal of cardiovascular electrophysiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.193
H-Index - 138
eISSN - 1540-8167
pISSN - 1045-3873
DOI - 10.1111/j.1540-8167.2006.00378.x
Subject(s) - medicine , gating , stimulation , sodium channel , sodium , biophysics , intracellular , ion channel , cardiology , endocrinology , chemistry , physiology , biochemistry , biology , receptor , organic chemistry
In the first section of this short review the change of the cardiac action potential (APD) with the rate of stimulation under physiological conditions is described and mechanistically analyzed. A fast phase of adaptation is mainly caused by changes in gating characteristics of ionic currents, and rapid modulation of the Na + /Ca 2+ exchanger. The slower phase is largely conditioned by incomplete recovery from inactivation of the late Na + current (late I Na ) and changes in ion concentrations of [K + ] e , [Na + ] i , and [Ca 2+ ] i , which cause secondary changes in the permeation and the gating of ion channels and flux through transporters. In a second section, an analysis is presented of the rate dependence of APD in pathological conditions and its importance in the genesis of arrhythmias in hypertrophy, heart failure, congenital, and acquired LQT syndromes is summarized. The role of the late I Na , Na + , and Ca 2+ overload is emphasized. Special attention is given to the paradoxical transient lengthening of APD in LQT3 syndrome for the sudden increase in rate in this setting. The third section consists of a short commentary on Na + and Ca 2+ overload and drugs which block the late I Na .