The nucleus of the solitary tract (NTS) is an important area of the brainstem that receives and integrates afferent cardiorespiratory sensorial information, including those from arterial chemoreceptors and baroreceptors. It was described that
acetylcholine (ACh) in the commissural subnucleus of the NTS (cNTS) promotes an increase in the phrenic nerve activity (PNA) and antagonism of
nicotinic receptors in the same region reduces the magnitude of tachypneic response to peripheral chemoreceptor stimulation, suggesting a functional role of
cholinergic transmission within the cNTS in the chemosensory control of respiratory activity. In the present study, we investigated whether
cholinergic receptor antagonism in the cNTS modifies the sympathetic and respiratory reflex responses to
hypercapnia. Using an arterially perfused in situ preparation of juvenile male Holtzman rats, we found that the nicotinic antagonist (
mecamylamine, 5 mM), but not the
muscarinic antagonist (
atropine, 5 mM), into the cNTS attenuated the
hypercapnia-induced increase of hypoglossal activity. Furthermore,
mecamylamine in the cNTS potentiated the generation of late-expiratory (late-E) activity in abdominal nerve induced by
hypercapnia. None of the
cholinergic antagonists microinjected in the cNTS changed either the sympathetic or the phrenic nerve responses to
hypercapnia. Our data provide evidence for the role of
cholinergic transmission in the cNTS, acting on
nicotinic receptors, modulating the hypoglossal and abdominal responses to
hypercapnia.