Blood flow is redistributed from the viscera to the periphery during periods of heat stress in order to maximize heat loss. The heat-induced redistribution of blood flow is strongly influenced by non-thermal inputs such as hydration status. At present little is known about where thermal and non-thermal information is integrated to generate an appropriate effector response. Recently the periventricular tissue that surrounds the anteroventral third ventricle (AV3V) has been implicated in the integration of thermal and osmotic information. The purpose of the present study was to determine the effects of electrolytic lesions of the AV3V on the cardiovascular response to a passive heat stress in conscious, free-moving male Sprague-Dawley rats. Core temperature was elevated at a constant rate of ~0.03°C/min in sham- and AV3Vlesion rats using an infra-red heat lamp. Changes in mesenteric and hindquarter vascular resistance were determined using Doppler flow probes and heat induced salivation was estimated using the spit print technique. The rise in mean arterial pressure (MAP), heart rate (HR) and mesenteric resistance in response to elevations in core temperature were all attenuated in AV3Vlesion rats, however hindquarter resistance was unaffected. Heat-induced salivation was also diminished. In addition, AV3V-lesion rats were more affected by the novelty of the experimental environment, resulting in a higher basal core temperature, HR and MAP. These results indicate that AV3V lesions disrupt the cardiovascular and salivatory response to a passive heat stress in rats and produce an exaggerated stress-induced fever triggered by a novel environment.