Estudo da neurotransmissão do quimiorreflexo e do barorreflexo na área A5 de ratos não anestesiados

Abstract

The circulatory system is essential for the maintenance of body homeostasis. Neural regulation of the cardiovascular system involves the activation of several groups of peripheral sensors that generates the information to central nervous system, with consequent modulation of the autonomic nervous system. Among the peripheral sensors the arterial baroreceptors, the cardiopulmonary receptors and the peripheral chemoreceptors can be highlighted. The A5 area is a region localized in the brainstem, more precisely in the pons, and is comprised of noradrenergic neurons. Neuroanatomy studies have identified connections between the A5 area and several areas involved in cardiovascular control. Previous studies conducted in our laboratory demonstrated that stimulation of the A5 area produced large pressor response and tachycardia. Additionally, this study demonstrated the essential role of this area in the chemoreflex pressor component in unanesthetized rats. Other studies have demonstrated that alterations in arterial pressure modified the spontaneous activity of the A5 area neurons, in within modifications depends of baroreceptor afferent input integrity. However, the role of the A5 area in the integration of baroreflex responses in unanesthetized rats still needs to be further investigated.Moreover, we evaluated the neurotransmission of the chemoreflex sympatho-excitatory component within the A5 area, as well, we evaluated the participation of this area in the cardiac baroreflex regulation, in unanesthetized rats. In our findings, both the ionotropic glutamatergic antagonist kynurenic acid, as well as the metabotropic glutamatergic antagonist MCPG, did not altered cardiovascular responses induced by chemoreflex stimulation. We also demonstrated that the blockade of gabaergic receptors of the A5 area did not result in alterations in basal arterial pressure. Additionally, this blockade did not alter the chemoreflex pressor response, suggesting that the sympatho-excitatory neurotransmission in the 16 A5 area does not occur through disinhibition of these neurons. Other findings from the present study indicate that the sensitivity of baroreflex bradycardia as well as the baroreflex tachycardia was not altered after the inhibition of the A5 area. Together these results indicate that the L-glutamate neurotransmitter was not involved in the integration of the sympatho-excitatory component of the chemoreflex response. Our data also showed that the A5 area does not participate in baroreflex control of heart rate.