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Acute exposure to thyroid hormone increases Na⁺ current and intracellular Ca²⁺ in cat atrial myocytes

Yong G. Wang, Elena N. Dedkova, Jon P. Fiening, Kaie Ojamaa *, Lothar A. Blatter and Stephen L. Lipsius

Whole-cell recording methods and fluorescence microscopy were used to study the effects of acute exposure to thyroid hormone (T₃) on cat atrial myocytes. Acute exposure (~5 min) to 10 nM T₃ significantly increased tetrodotoxin (TTX)-sensitive inward Na⁺ current (I_Na) at voltages between -40 and +20 mV. At maximal I_Na activation (-40 mV) T₃ increased peak I_Na by 32 %. T₃ had no effect on the time course of I_Na decay, voltage dependence of activation, inactivation, or recovery from inactivation. Comparable exposures to reverse T₃ (rT₃) or T₄ had no effect on I_Na. L-type Ca²⁺ current was unaffected by acute exposure to T₃. T₃-induced increases in I_Na were unaffected by 50 µM nickel, a blocker of T-type Ca²⁺ current. T₃ significantly increased cell shortening (+62 %) and could elicit spontaneous action potentials arising from Ca²⁺-mediated after-depolarizations. T₃ (but not rT₃) significantly increased baseline intracellular Ca²⁺, release of Ca²⁺ from sarcoplasmic reticulum (SR) and caffeine (10 mM)-induced release of SR Ca²⁺. We conclude that acute T₃ exposure increases Na⁺ influx via I_Na and thereby stimulates reverse-mode Na⁺-Ca²⁺ exchange to increase intracellular Ca²⁺ content and release. As a result, T₃ increases contraction strength, and can initiate Ca²⁺-mediated arrhythmic activity. Acute non-genomic effects of T₃ can contribute to the positive inotropy and sinus (atrial) tachycardia traditionally attributed to chronic, genomic effects of elevated thyroid hormone on atrial muscle.

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