To investigate the sequence and nature of the peripheral vascular responses during the prodromal period of heat stroke, rats were implanted with Doppler flow probes on the superior mesenteric (SMA), left iliac (LIA) or left renal (LRA), and external caudal (ECA) arteries. Studies were performed in unanesthetized rats (n = 6) exposed to 46 degrees C and in chloralose-anesthetized animals (n = 11) at 40 degrees C. Core (Tc) and tail-skin temperatures, heart rate, and mean arterial blood pressure (MAP) were also monitored. In both groups, prolonged (70-150 min) exposure progressively elevated Tc from 37.0 to 44.0 degrees C. MAP rose to a plateau then fell precipitously as Tc exceeded 41.5 degrees C. SMA resistance increased throughout the early stages of heating, with a sharp decline from this elevated level 10-15 min before the precipitous fall in MAP. ECA resistance fell initially but increased in the terminal stage of heating. In unanesthetized animals, LIA resistance progressively declined. In chloralose-anesthetized animals LRA resistance rose progressively, then increased markedly as Tc exceeded 41.5 degrees C. These data support the hypothesis that a selective loss of compensatory splanchnic vasoconstriction may trigger the cascade of events that characterize heat stroke. This differential vascular response was similar in both unanesthetized and anesthetized animals.