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

Whole‐cell recording methods and fluorescence microscopy were used to study the effects of acute exposure to thyroid hormone (T 3 ) on cat atrial myocytes. Acute exposure (≈5 min) to 10 n m T 3 significantly increased tetrodotoxin (TTX)‐sensitive inward Na + current ( I Na ) at voltages between −40 and +20 mV. At maximal I Na activation (−40 mV) T 3 increased peak I Na by 32 %. T 3 had no effect on the time course of I Na decay, voltage dependence of activation, inactivation, or recovery from inactivation. Comparable exposures to reverse T 3 (rT 3 ) or T 4 had no effect on I Na . L‐type Ca 2+ current was unaffected by acute exposure to T 3 . T 3 ‐induced increases in I Na were unaffected by 50 μ m nickel, a blocker of T‐type Ca 2+ current. T 3 significantly increased cell shortening (+62 %) and could elicit spontaneous action potentials arising from Ca 2+ ‐mediated after‐depolarizations. T 3 (but not rT 3 ) significantly increased baseline intracellular Ca 2+ , release of Ca 2+ from sarcoplasmic reticulum (SR) and caffeine (10 m m )‐induced release of SR Ca 2+ . We conclude that acute T 3 exposure increases Na + influx via I Na and thereby stimulates reverse‐mode Na + ‐Ca 2+ exchange to increase intracellular Ca 2+ content and release. As a result, T 3 increases contraction strength, and can initiate Ca 2+ ‐mediated arrhythmic activity. Acute non‐genomic effects of T 3 can contribute to the positive inotropy and sinus (atrial) tachycardia traditionally attributed to chronic, genomic effects of elevated thyroid hormone on atrial muscle.