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ABSTRACT: Background
Heart failure (HF) is characterized by electrophysiological remodeling resulting in increased risk of cardiac arrhythmias. Previous reports suggest that elevated inward ionic currents in HF promote action potential (AP) prolongation, increased short-term variability of AP repolarization, and delayed afterdepolarizations. However, the underlying changes in late Na+ current (INaL), L-type Ca2+ current, and NCX (Na+/Ca2+ exchanger) current are often measured in nonphysiological conditions (square-pulse voltage clamp, slow pacing rates, exogenous Ca2+ buffers).Methods
We measured the major inward currents and their Ca2+- and β-adrenergic dependence under physiological AP clamp in rabbit vent
SUBMITTER: Hegyi B
PROVIDER: S-EPMC6720130 | biostudies-literature | 2019 Mar
REPOSITORIES: biostudies-literature