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The effect of sympathetic activity on T4 and T3 levels in cold-exposed rats was investigated. Administration of the highest dose of propranolol (2 mg/100 g b.w.) twice daily during 4 days decreased T4 and T3 concentrations in plasma of rats living at 23°C (T4 from 46.4 ± 2.6 to 25.8 ± 5.3 nmol/l and T3 from 1.08. ± 0.6 to 0.82 ± 0.12 nmol/l). No significant effect on T4 and T3 levels (49.0 ± 11.6 and 1.48 ± 0.16 n/mol, respectively) after the administration of the same dose regimen of propranolol was observed in rats exposed to cold for 4 weeks. T4 and T3 levels in rats exposed to cold for 4 weeks were not significantly altered 1 week after sympathectomy, while remaining in the cold. However, chemical sympathectomy before cold exposure delayed the cold induced T3 elevation occurring during the first week of cold exposure (controls: from 1.16 ± 0.19 to 1.44 ± 0.29 nmol/l; sympathectomized rats: from 1.07 ± 0.12 to 1.17 ± 0.22 nmol/l). After 2 weeks of cold exposure the T3 levels of controls and sympathectomized rats were not significantly different (controls: 1.45 ± 0.12 nmol/l, sympathectomized rats: 1.38 ± 0.15 nmol/l). No effect of sympathectomy was observed on T4 levels. These experiments show that the role of sympathetic activity in increasing T3 is not clear during cold exposure. They provide some evidence that sympathetic activity may play a role in the initiation of the process leading to increased T3 plasma levels during cold exposure.

The ability of noradrenaline (1 microM), phenylephrine (10 microM), and isoproterenol (1 microM) to stimulate glycogenolysis in euthyroid and hypothyroid perfused rat livers was investigated. It was found that hypothyroidism severely impaired alpha-receptor-mediated (noradrenaline, phenylephrine) glucose release. The initial Ca2+ efflux and K+ influx induced by these agonists in the euthyroid control group were almost totally absent in the hypothyroid group, while glycogen phosphorylase a activity in the hypothyroid rat livers was markedly lower than in the controls after infusing noradrenaline for 1 min. Diminished CA2+ efflux (and possibly diminished K+ influx) is likely to play a role in the large impairment in the action of noradrenaline or phenylephrine on glycogenolysis in the perfused hypothyroid rat liver. After prolonged stimulation (15 min) with noradrenaline, however, the phosphorylase a activity in the hypothyroid and euthyroid groups did not differ significantly. This was accompanied by Ca2+ influx in the hypothyroid livers, probably facilitated by a beta-adrenergic effect of noradrenaline in this group. Hypothyroidism potentiated the effect of isoproterenol on glycogenolysis. The glucose 6-phosphate content in the hypothyroid rat livers was markedly higher than in the euthyroid group after stimulation by noradrenaline or isoproterenol.

The effect of experimental hyperthyroidism on skeletal muscle metabolism during force development and subsequent recovery was studied in a perfused preparation of the gastrocnemius and plantaris muscle of rats. After equilibration, the muscles were stimulated for 15 minutes at 1 Hz, and were allowed to recover during the following 15 minutes. The basal oxygen consumption of the skeletal muscle preparation was increased by 40% in the hyperthyroid rats as compared with euthyroid rats. The results show that: 1. Active force at 1 Hz was significantly reduced in the hyperthyroid rats compared with euthyroid rats, but the decay of force was similar in the two groups. 2. The increase in oxygen and glucose consumption and in lactate production during stimulation of the muscles was equal in hyperthyroid and euthyroid rats, but during recovery, oxygen consumption was significantly higher in the hyperthyroid than in euthyroid rats. 3. The increase in ATP turnover during force development and recovery (calculated from changes in O2 uptake, lactate production, and the breakdown of creatine-phosphate) in relation to the sum of force was significantly increased in the hyperthyroid state.