The influence of environmental heat stress on the arterial baroreflex control of heart rate (HR) was studied in eight conscious, chronically instrumented baboons. Inflations of balloon occluders around the inferior vena cava (IVC) and thoracic descending aorta (DA) were used to produce acute, graded changes in mean arterial blood pressure (MABP) in 5 mm Hg intervals ranging from +/- 5 to +/- 25 mm Hg. After determination of the HR responses to changes in MABP in the normothermic baboon (blood temperature less than or equal to 37.6 degrees C), the animal was subjected to environmental heating to produce hyperthermia. When blood temperature reached approximately 39.5 degrees C, HR responses to graded DA and IVC occlusions were again determined. During hyperthermia, the HR sensitivity (delta HR/ delta MABP) to MABP changes was markedly diminished for reductions in MABP and significantly enhanced for increases in MABP. To determine whether these alterations in the HR response to changes in MABP were due to an alteration of the baroreflex control of HR, full, sigmoid-shaped HR-MABP curves for both the normothermic and hyperthermic states were constructed and characterized by total HR range, estimated slope of the steep portion of the curve, and MABP at the midpoint of the HR range (BP50). During hyperthermia (1) the whole HR-MABP curve shifted significantly upward by 35-40 beats/min, (2) total HR range, the estimated slope, and BP50 did not change, and (3) the control point (pre-occlusion HR-MABP value) curves were also constructed during either beta-adrenergic blockade or cholinergic (Ch)-receptor blockade in the normothermic and hyperthermic state. Similar to that seen for the unblocked heart, the whole HR-MABP curves were also shifted upward during hyperthermia in this group of baboons with no alteration in the total HR range, the estimated slope, or BP50. The upward shift in the HR-MABP curve during Ch-receptor blockade, unlike during beta-receptor blockade, was much greater than that which could be attributed only to the local effect of blood temperature. Although the control point was also shifted upward along the steep portion of the curve during beta- or Ch-receptor blockade, the upward shift observed during beta-adrenergic blockade was similar to that observed in the unblocked state. Thus, a heat stress-induced hyperthermia produces a rise in HR without significantly altering the characteristics of the reflex control of HR by arterial baroreceptors. To rely solely on changes in HR sensitivity may lead to erroneous conclusions as to the effect of a particular stress on the baroreceptor reflex control of HR. Further, these results indicate that: (1) the upward shift in the HR-MABP curve is mediated by both the local effect of blood temperature on HR and cardiac sympathetic efferent neurons which are independent of the baroreceptor reflex, and (2) the upward shift in the control point is mediated predominantly by vagal withdrawal, probably as part of the compensatory response to a heat-induced hypotension.