To elucidate the contribution of cardiopulmonary baroreflexes on the control of total peripheral vascular conductance (TVC) during hyperthermia, alpha-chloralose-anesthetized rats with (VX-groups) or without (C-groups) vagotomy were subjected to body heating raising arterial blood temperature (Tb) at a rate of 0.1 degree C/min. In both the C- and VX-groups, rats were divided into normovolemia (C-NBV and VX-NBV) and furosemide-induced hypovolemia (C-LBV and VX-LBV) and cardiovascular responses to hyperthermia were compared between the four groups. Central venous pressure (CVP) decreased as Tb rose to 43 degrees C by 1.92 +/- 0.24, 1.36 +/- 0.28, 0.62 +/- 0.14, and 0.35 +/- 0.23 mmHg in the C-NBV, VX-NBV, C-LBV, and VX-LBV groups, respectively. Mean arterial pressure increased by 35-45 mmHg in the C-groups and by 25-35 mmHg in the VX-groups at Tb of 42-43 degrees C in the C-groups and 42 degrees C in the VX-groups. Heart rate response to increased Tb was not affected by vagotomy or LBV. Stroke volume correlated with CVP (r = 0.769) and this relationship did not differ among the four groups. TVC was more highly correlated with CVP in the C-groups (r = 0.925) than in the VX-groups (r = 0.757). The slope of TVC vs. CVP (TVC/CVP) for the VX-groups lowered by about 40% from that for the C-groups. These results suggest that during hyperthermia, cardiopulmonary baroreflexes may partly contribute to the control of TVC, and other mechanisms related to decreased BV and increased Tb play some roles in the control of TVC.