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1. In brown adipose tissue, noradrenaline induces an increase in respiration and a depolarization of the cells. The effect of an increase in potassium concentration in a range known to depolarize the brown adipocytes was tested on the O2 consumption. 2. Isolated interscapular brown adipose tissue from the rat was incubated in chambers that allowed O2 consumption to be measured over prolonged periods. 3. 45-50 mM-KC1 were found to induce a more that fourfold increase in O2 consumption, which was stable, reversible and dependent upon the presence of calcium in the meduim. 4. When rats were pre-treated with reserpine or 6-hydroxydopamine the KC1-induced increase in O2 consumption was sharply reduced or entirely adsent. 5. The effect of KC1 was greatly inhibited by (-)-propranolol, but not by (+)-propranolol. 6. Moderate increases in O2 consumption induced by low concentrations of potassium were potentiated by desipramine, a drug which is known to block the uptake of catecholamines by adrenergic nerve endings. 7. Surgical denervation caused a decrease in the catecholamine content of the tissue, but had no effect on the KC1 response. 8. It is concluded that in brown adipose tissue, potassium stimulates O2 consumption by causing a release of noradrenaline from nerve endings. This implies that surgical denervation as it is commonly performed on this tissue does not denervate the brown adipocytes but probably only the blood vessels.

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