A total of 12 experiments was done in cold-adapted (C-A) and warm-adapted (W -A) beagle dogs, kept more than 40 days at -10° C and 28° C, respectively. The animals, anesthetized with pentobarbital sodium (30 mg/kg), were paralyzed with Flaxedil (5 mg/kg/hour) and mechanically ventilated at 28-30° C. Oxygen consumption, heart rate and colonic, pinna and paw skin temperatures were measured continuously. The dogs were infused with noradrenalin (1.25 µg/kg/min) for 20 minutes at 30° C and after 45 minutes of acute cold exposure to 5° C. At 28-30° C, basal O2 consumption was higher in C-A dogs. Oxygen consumption of C-A dogs increased with a slight', increase in the heart rate during the initial 18-20 minutes after body cooling and then decreased. In W-A dogs, O2 consumption decreased continuously after acute cold exposure. Calorigenic effects of infused noradrenalin were consistent in C-A and W-A dogs at 30° and 5° C, but there was no difference between the increased amount of O2 consumption from the initial levels in both groups. Noradrenalin caused an increase of the heart rate in W-A dogs at 30° and 5° C, with decrease or no change in C-A dogs. Colonic, pinna and paw skin temperatures were significantly higher in C-A than in W-A dogs. Noradrenalin caused an increase in the temperatures, but the effect of the drug was more prominent in W-A than in C-A animals at lower temperature. These results suggest that the mechanism of nonshivering heat production is well developed by cold acclimation in dogs, and that the increase of this mechanism is due rather to the increase of noradrenalin content in blood than to increased sensitivity of the animals to the calorigenic effects of noradrenalin.