Control of sympathetic neuron and cardiovascular effector activity by carbon dioxide

The effect of CO$ sb2$ on sympathetic preganglionic neuron (SPN) activity and hindlimb neurogenic vascular resistance (HVR) was investigated in cats. Both variables increased as continuous functions of systemic arterial PCO$ sb2$, from hypocapnia to hypercapnia. Eucapnic PCO$ sb2$ was responsible for a significant component of SPN background activity and HVR. The carotid body chemoreceptors were shown to contribute to the CO$ sb2$ response of SPNs, since section of the carotid sinus nerves, after prior section of the aortic nerves, reduced the CO$ sb2$ response of SPNs. A significant ventral medullary contribution to this CO$ sb2$ relationship was demonstrated, since the CO$ sb2$ response persisted after peripheral chemodenervation, was lost after acute spinal transsection and was markedly attenuated by cold-block of either the entire exposed ventral surface of the medulla or the specific bilateral area "S". Superficial ventral medullary chemoreceptor involvement was confirmed, since changes in HVR, comparable to those caused by altering arterial PCO$ sb2$, occurred with changes in the (H$ sp+$) and PCO$ sb2$ in artificial CSF perfusing these structures