We have used a telemetry system to record heart rate, body temperature, electrocardiogram (ECG), and locomotor activity in awake, freely moving mice lacking thyroid hormone receptor (TR)- or TR-₁ and - (TR-₁/). The TR-₁/-deficient mice had a reduced heart rate compared with wild-type controls. The TR--deficient mice showed an elevated heart rate, which, however, was unresponsive to thyroid hormone treatment regardless of hormonal serum levels. ECG revealed that the TR--deficient mice had a shortened Q-T_end time in contrast to the TR-₁/-deficient mice, which exhibited prolonged P-Q and Q-T_end times. Mental or pharmacological stimulation of the sympathetic nervous system resulted in a parallel increase in heart rate in all animals. A single injection of a nonselective -adrenergic-receptor blocker resulted in a parallel decrease in all mice. The TR-₁/-deficient mice also had a 0.4°C lower body temperature than controls, whereas no difference was observed in locomotor activity between the different strains of mice. Our present and previous results support the hypothesis that TR-₁ has a major role in determining heart rate under baseline conditions and body temperature and that TR- mediates a hormone-induced increase in heart rate.

knockout mice; heart rate; electrocardiogram

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