Blood flow was measured with labeled microspheres in cold (6 degrees C)- and room-temperature-acclimated rats at rest and during infusion of the beta-agonist, isoproterenol. Isoproterenol elicited decreased mass-specific blood flows (ml . g-1 . min-1) to liver (55% of control), kidney (48%), and white fat (64%) in room-temperature-acclimated (RT) rats. Blood flow was similarly decreased in liver (51%), kidney (37%), and white fat (70%) in cold-acclimated (CA) rats. In contrast, isoproterenol increased blood flows to brown fat and cardiac and skeletal muscles. The blood flows to cardiac muscle during isoproterenol infusion were comparable in both RT (12.7 ml . g-1 . min-1) and CA (11.7 ml . g-1 . min-1) animals, representing increases of 2.9- and 2.6-fold above control values, respectively. Blood flow to skeletal muscle was also similarly elevated in RT and CA animals, representing increases 5.9 and 5.6 times those of their respective control values. In contrast, although isoproterenol greatly stimulated (ca. 8-fold) blood flow to brown fat (interscapular plus cervical depots) in RT animals, it had a greater effect on these two depots in the CA rats (18-fold increase). These data emphasize the importance of brown fat as a major effector of nonshivering thermogenesis as well as the importance of beta-adrenergic receptors in mediating the metabolic response of nonshivering thermogenesis.