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Am J Physiol Regul Integr Comp Physiol 275: R640-R646, 1998;
0363-6119/98 $5.00
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Vol. 275, Issue 2, R640-R646, August 1998

Evidence that decreased heart rate in thyroid hormone receptor-alpha 1-deficient mice is an intrinsic defect

Catarina Johansson1, Björn Vennström2, and Peter Thorén1

1 Department of Physiology and Pharmacology and 2 Department of Cell and Molecular Biology, Karolinska Institute, S-171 77 Stockholm, Sweden

Using a telemetry system with implantable transmitters, we recorded heart rate, electrocardiogram (ECG), body temperature, and locomotor activity continuously in awake, freely moving mice deficient in the thyroid hormone receptor-alpha 1 (TRalpha 1). We have previously reported that the TRalpha 1-deficient mice have a 20% lower mean heart rate and a 0.5°C lower body temperature compared with wild-type control animals. In this study we found that when 3,5,3'-triiodothyronine (T3) was given once a day, there was a parallel increase in heart rate (occurring 1 day later in the TRalpha 1-deficient mice than in controls) and body temperature. Analysis of single-lead ECG revealed a prolonged QRS and Q-Tend time in the TRalpha 1-deficient mice, which was shortened after T3 treatment. Monophasic action potential durations, measured in hearts from anesthetized mice at 90% of repolarization, were significantly prolonged in TRalpha 1-deficient mice. Air-jet stress and a single injection of an anticholinergic agent induced a parallel increase, and a beta -adrenergic receptor blocker induced a decrease in heart rate in both groups. There was no difference in beta -adrenergic receptor density. The results indicate that the TRalpha 1-deficient mice have a specific defect in intrinsic heart rate regulation.

electrocardiogram; monophasic action potentials; body temperature; blood pressure


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