Role of carotid and central chemoreceptors in the CO2 response of sympathetic preganglionic neurons.

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In anesthetized, vagotomized, paralyzed, artificially ventilated cats with aortic nerves cut, we recorded the response of 28 sympathetic preganglionic neurons (SPNs) of the cervical sympathetic trunk of changes in arterial pCO2. We observed the effects on these responses of: (i) surgical denervation of carotid sinus chemoreceptors in normoxia (paO2 110 mm Hg); and (ii) hyperoxia (paO2 greater than 350 mm Hg) which is known to depress peripheral chemoreceptor sensitivity to CO2. Stimulus-response curves, obtained by rebreathing at constant paO2, were used to detect the effects of these manoeuvres. The present experiments have confirmed previous observations demonstrating the CO2-sensitivity of this neuron population. The population average firing rate, as a function of paCO2, describes a sigmoid curve, increasing continuously between 20 and 90 mm Hg and asymptotically approaching plateaus at the highest and lowest paCO2 values. Carotid sinus nerve section caused a decrease of the average response of the population at all paCO2 values, resulting in a displacement to the right of the response curve, in a decrease in slope and maximum values. On the assumption that the CO2 response curve after carotid sinus nerve section is due to central chemoreceptor input, and that there is a simple addition between the effects of central and carotid chemoreceptors, the difference between CO2 response curves ("difference curves") before and after denervation represents the contribution of the carotid chemoreceptors. A comparison of this "difference curve" with the curve obtained after denervation reveals that the contribution of the carotid chemoreceptors is of the same magnitude as that of the central chemoreceptors up to a paCO2 value of 60-70 mm Hg. Beyond this value, the carotid contribution declines and becomes a smaller component of the total response, whereas the contribution of the central chemoreceptors continues to increase. Similar results were obtained with rebreathing in hyperoxia, after correction for the central excitatory effect of hyperoxia. Hyperoxia never caused a depression of the CO2 response of units after section of the carotid sinus nerve. Observation of the effects of the two manoeuvres on individual SPNs leads to the conclusion that in approximately half of the CO2-sensitive units there is an overlap of central and peripheral chemoreceptor input. The remainder of the CO2-sensitive units receive input only from the central chemoreceptors.