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Am J Physiol Regul Integr Comp Physiol (December 5, 2002). doi:10.1152/ajpregu.00310.2002
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Articles in PresS, published online ahead of print December 5, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00310.2002
Submitted on May 29, 2002
Accepted on November 27, 2002

Pressor response to chemoreflex activation before and after microinjection of glycine into the NTS of awake rats

Franklin F Pimentel1, Leni G. H Bonagamba1, and Benedito H Machado1*

1 Physiology, University of Sao Paulo, Ribeirao Preto, Sao Paulo, Brazil

* To whom correspondence should be addressed. E-mail: bhmachad{at}fmrp.usp.br.

Microinjection of glycine into the rostral (bilateral) and caudal (midline) commissural NTS using 3 guide cannulas implanted in the direction of these sites produced an increase in mean arterial pressure (MAP) and abolished the pressor response to chemoreflex activation [KCN (n=7)]. Strychnine, a glycine receptors antagonist, attenuated the increase in MAP and in this new experimental condition (n=5) the pressor response to chemoreflex activation was not altered. Considering that the effect of glycine on the attenuation of the pressor response to chemoreflex activation could be secondary to the increase in baseline MAP, in a third group of rats (n=5) sodium nitroprusside infusion (iv) after microinjections of glycine into the NTS normalize MAP. In this case the pressor response to chemoreflex activation was similar to the control. The data shows that glycine when microinjected bilaterally into the lateral commissural NTS as well as into the medial commissural NTS plays no major inhibitory role in the processing of the neurotransmission of the sympathoexcitatory component of the chemoreflex.




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