Heart-rate (HR) and systolic-pressure (SP) responses to unilateral and bilateral carotid occlusion (BCO) and to central vagal stimulation were measured in control anesthetized dogs, after bilateral vagotomy, and after extensive disruption of the neuraxis by RF lesions. Preocclusion HR was significantly increased after vagotomy, with no change in SP. Lesions had no effect on resting HR, but they decreased SP. HR response to BCO was unchanged after vagotomy, but decreased almost 50% after lesions. The SP response to BCO increased greatly after vagotomy and returned to control levels after lesions. The response in HR and SP to unilateral right carotid occlusion (RCO) was larger than that to left carotid occlusion (LCO) under all experimental conditions. The summed response to RCO + LCO did not equal the BCO response. Supramaximal stimulation of the left central vagus evoked larger responses in HR and SP than the right vagus before lesions, but only HR responses were larger after lesions. It is suggested that the integrative mechanisms involved have some independent central connections, and that they are modulated by a complex control system which includes CNS levels above the mesencephalon.