Central chemoreceptors and neural mechanisms of cardiorespiratory control. T.S. Moreira, A.C. Takakura, R.S. Damasceno, B. Falquetto, L.T. Totola, C.R. Sobrinho, D.T. Ragioto and F.P. Zolezi. Braz J Med Biol Res 2011; 44: 883-889.

Figure 2. Scheme showing the contribution of the RTN to the central sympathetic chemoreflex. Signals from central or peripheral chemoreceptors may directly or indirectly affect the activity of several medullary areas, including the RTN, NTS, RVLM, and CPG, which affect sympathetic discharge to heart and blood vessels and to respiratory muscles. An essential step for motor neuron hypercapnia-induced phrenic nerve activity is activation of RTN neurons by CO2/H+, which in turn send excitatory signals to activate the CPG, either directly or through activation of metabotropic and ionotropic glutamate receptors in the RVLM. Signals from the RTN that activate metabotropic receptors in the RVLM may also increase sympathetic activity to the cardiovascular system (24). CPG = central pattern generator; commNTS = commissural nucleus tractus solitarii; IgluR = glutamatergic ionotropic receptors;
MgluR = glutamatergic metabotropic receptors; RTN = retrotrapezoid nucleus; RVLM = rostral ventrolateral medulla; SPGn = sympathetic preganglionic neurons.