INHIBITION OF CHEMORECEPTOR INPUTS TO NUCLEUS OF TRACTUS-SOLITARIUS NEURONS DURING BARORECEPTOR STIMULATION

The reflex effects of arterial chemoreceptor activation are attenuated as arterial pressure is elevated and augmented as arterial pressure is decreased. This study was designed to test the hypothesis that excitatory arterial chemoreceptor inputs to neurons in the nucleus tractus solitarius (NTS) are inhibited by arterial baroreceptors. In pentobarbital sodium-anesthetized, mechanically ventilated, paralyzed cats, extracellular recordings were obtained from NTS neurons, which were excited after brief activation of ipsilateral carotid body chemoreceptors. During increases in arterial pressure, carotid sinus nerve (CSN)-evoked discharge was 45-112% of the control-evoked discharge at the prevailing level of arterial pressure (n = 70). Inhibition of CSN-evoked discharge during increased arterial pressure was significant when evoked discharge was <90% of control (n = 31; 67 +/- 2%, mean percent of control-evoked discharge +/- SE; P < 0.01, Wilcoxon signed-rank test). The inhibition of CSN-evoked discharge was reduced after section of both vagi, both aortic nerves, and the contralateral CSN (n = 5, P < 0.05). These results demonstrate that activation of arterial baroreceptors attenuates excitatory chemoreceptor inputs to a subpopulation of NTS neurons. The inhibition appears to be mediated by disfacilitation. The results indicate that baroreceptor modulation of arterial chemoreflexes occurs at an early stage of the reflex arc, within the NTS. The results also suggest that sympathoinhibition evoked by baroreceptors might include, as a component, reduced sympathoexcitatory, i.e., chemoreceptor, drive.