In the present study, we evaluated the role of glutamatergic mechanisms in the retrotrapezoid nucleus (RTN) in changes of splanchnic sympathetic nerve discharge (sSND) and phrenic nerve discharge (PND) elicited by central and peripheral chemoreceptor activation. Mean arterial pressure (MAP), sSND and PND were recorded in
urethane-anaesthetized, vagotomized, sino-aortic denervated and artificially ventilated male Wistar rats.
Hypercapnia (10% CO(2)) increased MAP by 32 ± 4 mmHg, sSND by 104 ± 4% and PND amplitude by 101 ± 5%. Responses to
hypercapnia were reduced after bilateral injection of the
NMDA receptor antagonist d,l-2-amino-5-phosphonovalerate (AP-5; 100 mm in 50 nl) in the RTN (MAP increased by 16 ± 3 mmHg, sSND by 82 ± 3% and PND amplitude by 63 ± 7%). Bilateral injection of the non-
NMDA receptor antagonist 6,7-dinitro-quinoxaline-2,3-dione (
DNQX; 100 mm in 50 nl) and the metabotropic receptor antagonist (+/-)-α-methyl-4-
carboxyphenylglycine (MCPG; 100 mm in 50 nl) in the RTN did not affect sympathoexcitatory responses induced by
hypercapnia. Injection of
DNQX reduced
hypercapnia-induced phrenic activation, whereas MCPG did not. In animals with intact carotid chemoreceptors, bilateral
injections of AP-5 and
DNQX in the RTN reduced increases in MAP, sSND and PND amplitude produced by
intravenous injection of NaCN (50 μg kg(-1)). Injection of MCPG in the RTN did not change responses produced by NaCN. These data indicate that RTN ionotropic glutamatergic receptors are involved in the sympathetic and respiratory responses produced by central and peripheral chemoreceptor activation.