Abstract
Acute treatment with near-physiological concentrations (20 nM) of thyroid hormone (3,5,3′-triiodo-L-thyronine; T3) prolonged inward sodium currents in neonatal rat cardiomyocytes. Lidocaine (10μM) rapidly reversed the T3 effects. A model of macroscopic sodium current including both fast and slow modes for activation as well as inactivation was developed to describe T3-dependent whole cell currents. These results suggest that T3 alters both the activation (m) and inactivation (h) processes of the Na channel.
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