The relative contribution of several effector systems to a prostaglandin E1-(PGE1) evoked hyperthermia was examined. Infusion of 150 ng of PGE1 into a lateral cerebral ventricle increased core temperature and whole body metabolic rate, brown adipose tissue temperature, systolic blood pressure, and heart rate. Pretreating the animals with a nonselective beta-antagonist propranolol (1 mg/kg iv in 0.3 ml followed by 3 mg.kg-1.h-1 in 0.3 ml/h) not only attenuated the rise in metabolism observed after the central administration of 150 ng PGE1 but also diminished the elevation in both core and brown fat tissue temperatures as well as the increase in heart rate. Pretreating the animals with the alpha-antagonist prazosin (2 mg/kg im followed by 50 micrograms.kg-1.h-1 iv in 0.3 ml/h) somewhat reduced the rise in whole body metabolism, suppressed the elevation in core temperature, but failed to alter the rise in brown adipose tissue temperature normally seen after the central administration of PGE1. Moreover, both the rise in systolic blood pressure and heart rate were attenuated when the PGE1 administration was preceded by prazosin. These results suggest that brown adipose tissue is an important effector organ responsible for mediating the hyperthermic response observed after the intracerebral injection of PGE1. In addition, the results indicate that alterations in vasomotor tone may also be important in producing or sustaining the elevated core temperature found after a pyrogen administration.