Sympathoexcitatory neurotransmission of the chemoreflex in the NTS of awake rats

Cardiovascular responses to chemoreflex activation by potassium cyanide (KC N, 20 mu g/rat iv) were analyzed before and after the blockade of ionotropi c or metabotropic receptors into the nucleus of the solitary tract (NTS) of awake rats. Microinjection of ionotropic antagonists [6,7-dinitroquinoxali ne-2,3-dione or kynurenic acid (Kyn)] into the lateral commissural NTS (NTS lat), the midline commissural NTS (NTSmid), or into both (NTSlat+mid), prod uced a significant increase in basal mean arterial pressure, and the presse r response to chemoreflex activation was only partially reduced, whereas mi croinjection of Kyn into the NTSmid produced no changes in the presser resp onse to the chemoreflex. The bradycardic response to chemoreflex activation was abolished by microinjection of Kyn into the NTSlat or into NTSlat+mid but not by Kyn microinjection into the NTSmid. Microinjection of alpha-meth yl-4-carboxyphenylglycine, a metabotropic receptor antagonist, into the NTS lat or NTSmid produced no changes in baseline mean arterial pressure or hea rt rate or in the chemoreflex responses. These results indicate that 1) the processing of the parasympathetic component (bradycardia) of the chemorefl ex seems to be restricted to the NTSlat and was blocked by ionotropic antag onists and 2) the presser response of the chemoreflex was only partially re duced by microinjection of ionotropic antagonists and not affected by injec tion of metabotropic antagonists into the NTSlat or NTSmid or into NTSlat+m id in awake rats.