Endocrine stimulation of muscle nonshivering thermogenesis (NST) in ducklings was investigated in vitro using a perfused hindlimb preparation maintained at 25 degrees C. Effects of flow rate, norepinephrine (NE), epinephrine, and glucagon on perfused muscle oxygen consumption (MO2) and perfusion pressure were studied. Control ducklings (Cairina moschata, 5 wk old) reared at thermoneutrality (25 degrees C, TN) were compared with two age-matched groups exhibiting muscle NST in vivo: cold-acclimated ducklings (4 degrees C, 4 wk, CA) and glucagon-treated ducklings (103 nmol/kg twice-daily, intraperitoneally, GT). Basal MO2 was higher in CA than in TN or GT ducklings and increased in all groups with elevated flow rates. Catecholamines increased both MO2 and perfusion pressure. The maximal effect on MO2 was higher in CA (+ 36%) and GT ducklings (+ 43%) than in controls (+ 31%), but was associated with reduced vasoconstriction. Flow rate did not consistently potentiate the NE response. At high doses, catecholamines became inhibitory on MO2 while a monotonous increase of pressure was still observed. Glucagon, by contrast, slightly decreased both MO2 and pressure. This vasodilatory effect was greater in CA ducklings than controls in preconstricted preparations. In vivo, low-dose epinephrine induced a modest thermogenic effect (+ 10%) in CA ducklings. These findings showed that duckling muscle thermogenesis is directly stimulated in vitro by catecholamines but not by glucagon. Higher in vitro thermogenic effects of NE in ducklings that were expected to exhibit muscle NST in vivo suggests catecholamine involvement in muscle NST in vivo. Potential vascular control of avian muscle NST is discussed.