Nociceptive afferents selectively modulate the cardiac component of the peripheral chemoreceptor reflex via actions within the solitary tract nucleus.

Our previous findings showed that the nucleus of the solitary tract (NTS) mediated part of the tachycardia evoked during somatic noxious stimulation. Here, we investigated the interaction between somatic nociceptor- and peripheral chemoreceptor-evoked cardiac changes. We sought to determine whether this interaction occurred within the NTS, the primary site of termination of chemoreceptor afferents. In a working heart-brainstem preparation of rat, mechanical noxious activation of a forelimb evoked a tachycardia of 17.5+/-3 (mean+/-S.E.M.) b.p.m., whereas sodium cyanide (7-30 microg) stimulation of peripheral chemoreceptors produced a sub-maximal bradycardia of -140+/-15 b.p.m. During nociceptor stimulation the sodium cyanide-evoked bradycardia was attenuated to -42.6+/-12 b.p.m. but could be prevented by a multiple bilateral NTS microinjection of bicuculline (i.e. -173+/-18 b.p.m.). Furthermore, the activity of NTS neurones responding to peripheral chemoreceptor stimulation increased from 2.8+/-1.3 to 9.4+/-1.9 Hz during sodium cyanide injection (n=7; P<0.01). The latter response was attenuated reversibly to 2.9+/-0.9 Hz during simultaneous stimulation of the brachial nerve. Pressure ejection of bicuculline abolished this inhibitory action of brachial-nerve stimulation on the chemoreceptor-evoked excitatory synaptic response. We conclude that somatic noxious stimulation attenuates the chemoreceptor reflex-evoked bradycardia via a GABA(A)ergic mechanism in the NTS.