Adrenergic beta-receptors and non-shivering thermogenesis.

Abstract

Sellers, Scott and Thomas1 demonstrated that after prolonged cold exposure (cold acclimatization) heat production through shivering is gradually replaced by an increase in non-shivering thermogenesis. It is often assumed that muscle tissue is an important site of non-shivering thermogenesis. Recently, Himms-Hagen2 has suggested that acceleration of the triglyceride cycle of brown adipose tissue is a major mechanism of non-shivering thermogenesis in cold-acclimatized rats. As lipid metabolism of adipose tissue is under β-adrenergic control, a study of the effect of β-adrenergic blockade on electrical muscle activity in rats exposed to about 4° C after acclimatization to 23° C or 4° C would be expected to yield valuable information. This communication presents preliminary data of such an investigation. Cold-acclimatized rats were removed from the cold room, anaesthetized with urethane (1 to 1.25 g/kg)—a drug known to alter only the degree, not the type, of the electrical response of muscle activity1—and exposed to a temperature of 4° C. Needle electrodes were inserted into a leg muscle and electrical activity was measured with a Grass model 5 polygraph3. Rectal temperature was monitored throughout the experiment. Each rat was tested at least twice, once when given drug treatment, and once when given saline or nothing. The β-adrenergic blocking agent, propranolol (AY 64043) (kindly donated by Ayerst, McKenna and Harrison, Ltd., Montreal), was used at doses of 0.3 or 0.9 mg/kg intraperitoneally every 30 min. Fig. 1 shows rectal temperature, duration of exposure to 4° C and the effect of the drug on electrical muscle activity in six cold-acclimatized rats. None of the animals shivered during an experimental period of 2.5 h when treated with saline. A seventh rat showed signs of shivering and was therefore excluded from this series. After treatment with propranolol, all six rats showed a marked increase of electrical muscle activity. Representative tracings of the muscle activity before and after propranolol are shown in Fig. 1: no effort was made to quantitate accurately the observed increase.