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Am J Physiol Heart Circ Physiol 278: H1105-H1116, 2000;
0363-6135/00 $5.00
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Vol. 278, Issue 4, H1105-H1116, April 2000

The thyroid hormone analog DITPA restores Ito in rats after myocardial infarction

Alan D. Wickenden, Roger Kaprielian, Xiao-Mang You, and Peter H. Backx

Departments of Physiology and Medicine and The Center for Cardiovascular Research, University Health Network, University of Toronto, Toronto, Ontario, Canada M5G 2C4

Previous studies have established that reductions in repolarizing currents occur in heart disease and can contribute to life-threatening arrhythmias in myocardium. In this study, we investigated whether the thyroid hormone analog 3,5-diiodothyropropionic acid (DITPA) could restore repolarizing transient outward K+ current (Ito) density and gene expression in rat myocardium after myocardial infarction (MI). Our findings show that Ito density was reduced after MI (14.0 ± 1.0 vs. 10.2 ± 0.9 pA/pF, sham vs. post-MI at +40 mV). mRNA levels of Kv4.2 and Kv4.3 genes were decreased but Kv1.4 mRNA levels were increased post-MI. Corresponding changes in Kv4.2 and Kv1.4 protein were also observed. Chronic treatment of post-MI rats with 10 mg/kg DITPA restored Ito density (to 15.2 ± 1.1 pA/pF at +40 mV) as well as Kv4.2 and Kv1.4 expression to levels observed in sham-operated controls. Other membrane currents (Na+, L-type Ca2+, sustained, and inward rectifier K+ currents) were unaffected by DITPA treatment. Associated with the changes in Ito expression, action potential durations (current-clamp recordings in isolated single right ventricular myocytes and monophasic action potential recordings from the right free wall in situ) were prolonged after MI and restored with DITPA treatment. Our results demonstrate that DITPA restores Ito density in the setting of MI, which may be useful in preventing complications associated with Ito downregulation.

action potential; transient outward current; Kv4.2; Kv4.3; Kv1.4; 3,5-diiodothyropropionic acid


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