Blood pressure and heart rate alterations were induced in anesthetized and unanesthetized mongrel dogs. Pressor responses were brought about in the anesthetized group by bilateral, high intensity stimulation of the sciatic nerves. In these animals, bilateral section of the dorsolateral sulcus area (DLS) in the lumbar spinal cord completely eliminated both blood pressure and heart rate responses to this stimulation. Baroreceptor-mediated bradycardia induced by pressor doses of phenylephrine was attenuated by sciatic nerve stimulation. Obliteration of this baroreceptor-somatic afferent interaction required ventrolateral extension of the bilateral spinal lesions to include both the DLS and the dorsolateral funiculus (DLF). Blood pressure and heart rate increments in unanesthetized dogs were induced by treadmill running. The pressor response to exercise was markedly increased by transient hind limb arterial occlusion during the course of the run. Surgical interruption of the ascending limb of the somato-autonomic reflex in the spinal cord of these animals (L1-L2 combined DLS and DLF lesion) significantly reduced the blood pressure response to simultaneous exercise-occlusion. These spinal lesions also reduced the heart rate response to treadmill running without occlusion. The descending pathways involved in autonomic reflexes appeared intact as the spinal lesions did not alter the blood pressure or heart rate response to bilateral carotid artery occlusion.