Is the central inspiratory activity responsible for pCO2-dependent drive of the sympathetic discharge?

Out of 27 cats anesthetized with chloralose-urethane mixture, paralyzed, vagotomized and artificially ventilated, phrenic nerve response to systemic hypercapnia (7-8 vol.% CO2/O2 mixture) was accompanied by an increase in blood pressure and sympathetic discharge in 19 cats. Out of these 19 cats, 12 were totally debuffered and in the remaining 7 cats one carotid sinus nerve was left intact. Single unit activity in the sympathetic cervical nerve and spontaneous mass activity in the cervical, splanchnic, renal sympathetic and phrenic nerves were recorded. Evoked response in the phrenic nerve was produced by electrical stimulation of the descending bulbospinal inspiratory pathways in the midplane area of the medulla or in the ventrolateral cervical spinal cord. Starting from the control mean end-tidal CO2 concentration of 4.7 vol.% (+/- 1.0 S.D.) a progressing hypocapnia was induced by hyperventilation up to the end-tidal CO2 concentration of 1.3-3.2 vol.% (mean 2.4 vol.% +/- 0.5 S.D.) significantly below paCO2 apneic threshold. In chemo- and baroreceptor denervated cats with a pressor and excitatory sympathetic response to hypercapnia, a hypocapnia resulted in a fall of the arterial blood pressure (mean 16.9 mm Hg +/- 7.5 S.D., 2.2 kpa +/- S.D.). With the increasing paCO2 over the period of hypocapnic apnea a pressor and excitatory sympathetic response preceded, in all experiments, the onset of the phrenic nerve rhythmic activity. The difference between paCO2 threshold for the pressor and sympathetic response (35.7 mm Hg +/- 3.6 S.D., 4.7 kpa +/- 0.5 S.D.) and paCO2 threshold for the reappearance of the phrenic nerve rhythmic activity (43.6 mm Hg +/- 2.6 S.D., 5.8 kpa +/- 0.3 S.D.) was highly significant. If apneic hypocapnia was combined with the continuous stimulation of the afferent fibers of the superior laryngeal nerve the CO2 threshold for phrenic rhythmic activity was significantly increased whereas CO2 threshold for the pressor and sympathetic excitatory response remained unchanged. CO2 administration during hypocapnia apnea caused a progressing reduction of the magnitude of the evoked phrenic nerve response. From these findings it is concluded that the central excitatory effect of CO2 on the sympathetic activity may be accomplished in the absence of the rhythmic respiratory activity and independently of the subthreshold tonic inspiratory activity. Pressor and sympathetic excitatory response to CO2 observed during hypocapnic apnea is presumably caused by a neuronal pool different from that responsible for the central inspiratory activity. It is suggested that this CO2 sensitive neuronal mechanism might be involved in the central generation of sympathetic tone.