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1 Department of Physiology and
Biophysics,
Cardiovascular
responses to chemoreflex activation by potassium cyanide (KCN, 20 µg/rat iv) were analyzed before and after the blockade of ionotropic
or metabotropic receptors into the nucleus of the solitary tract (NTS)
of awake rats. Microinjection of ionotropic antagonists
[6,7-dinitroquinoxaline-2,3-dione or kynurenic acid
(Kyn)] into the lateral commissural NTS
(NTSlat), the midline
commissural NTS (NTSmid), or
into both (NTSlat+mid), produced
a significant increase in basal mean arterial pressure, and the pressor
response to chemoreflex activation was only partially reduced, whereas
microinjection of Kyn into the
NTSmid produced no changes in the
pressor response 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
-methyl-4-carboxyphenylglycine, a metabotropic
receptor antagonist, into the
NTSlat or
NTSmid produced no changes in
baseline mean arterial pressure or heart rate or in the chemoreflex
responses. These results indicate that 1) the processing of the
parasympathetic component (bradycardia) of the chemoreflex seems to be
restricted to the NTSlat and was blocked by ionotropic antagonists and
2) the pressor response of the
chemoreflex was only partially reduced by microinjection of ionotropic
antagonists and not affected by injection of metabotropic antagonists
into the NTSlat or
NTSmid or into
NTSlat+mid in awake rats.
nucleus of the solitary tract; arterial chemoreceptors; cardiovascular regulation; N-methyl-D-aspartate
receptors; non-N-methyl-D-aspartate
receptors; metabotropic receptors; kynurenic acid; 6,7-dinitroquinoxaline-2,3-dione;
-methyl-4-carboxyphenylglycine
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