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Doctoral Thesis
DOI
https://doi.org/10.11606/T.41.2014.tde-16012015-112025
Document
Author
Full name
Sergio Marinho da Silva
E-mail
Institute/School/College
Knowledge Area
Date of Defense
Published
São Paulo, 2014
Supervisor
Committee
Chadi, Debora Rejane Fior (President)
Antunes, Vagner Roberto
Ferreira, Zulma Felisbina da Silva
Takakura, Ana Carolina Thomaz
Visconti, Maria Aparecida
Title in Portuguese
Modulação do sistema catecolaminérgico pelos receptores glutamatérgicos e de angiotensina II no bulbo de ratos
Keywords in Portuguese
Angiotensina II
Glutamato
Receptor α2 adrenérgico
Abstract in Portuguese
O controle neural da pressão arterial é essencial para a manutenção da homeostase do organismo. Este controle é realizado principalmente por núcleos bulbares e hipotalâmicos. Um dos principais sistemas de neurotransmissão envolvidos no controle da pressão arterial é o catecolaminérgico. Células noradrenérgicas e adrenérgicas estão presentes em todos os centros bulbares reguladores da pressão arterial, enquanto seus receptores, principalmente o receptor α2 adrenérgico (α2r), estão presentes nas mesmas regiões além de estarem presentes também nos núcleos hipotalâmicos. Estes receptores, quando ativados nestes núcleos, geram respostas cardiovasculares e atuam em conjunto com outros sistemas de neurotransmissão neste controle. Dentre estes sistemas de neurotransmissão, merecem destaque os sistemas angiotensinérgico e glutamatérgico, não apenas por estarem presentes nestes núcleos, mas também por atuarem no controle da pressão arterial. Contudo, pouco se sabe sobre como o sistema catecolaminérgico interage com estes sistemas. Desta forma, estudamos neste projeto a influência do sistema glutamatérgico e angiotensinérgico sobre o sistema catecolaminérgico no bulbo de ratos. Através de culturas de células bulbares, demonstramos que a ativação de receptores glutamatérgicos do tipo NMDA é capaz de elevar os níveis proteicos do α2R e que os receptores ionotrópicos do tipo não-NMDA precisam estar desbloqueados para tal. Em ratos adultos, microinjeções repetidas inibem a resposta bradicárdica induzida pela ativação dos α2rR no NTS. Contudo, o knockdown dos receptores AT1 de angiotensina restaura a resposta bradicárdica. A partir destes resultados, foi demonstrado que o sistema glutamatérgico é capaz de modular o sistema catecolaminérgico, enquanto o knockdown do receptor AT1 de angiotensina no NTS acentua a resposta bradicárdica dos α2R do NTS. Estes resultados sugerem que os sistemas de neurotransmissão bulbares interagem de diferentes formas e a compreensão deste controle pode vir a ser de grande valia para a compreensão de como se dá o controle da pressão arterial pelo sistema nervoso
Title in English
Modulation of the catecholaminergic system by glutamatergic and angiotensin II receptors in the rat medulla oblongata
Keywords in English
α2 adrenoceptor
Angiotensin II
Glutamate
Abstract in English
The neural control of blood pressure is essential for the maintenance of the homeostasis of the organism. This control is performed mainly by nuclei in the medulla oblongata and in the hypothalamus. One of the main neurotransmitter system involved in this control is the catecholaminergic. Noradrenergic and adrenergic cells are present in all medullary nuclei involved in the arterial pressure regulation, while its receptors, especially the α2 adrenoceptor, are present in the same region plus hypothalamic nuclei. These receptors, upon activation in these nuclei, generate cardiovascular response, and act with other neurotransmission systems in this control. Among these systems, the glutamatergic and angiotensinergic deserve attention not only for also being present in the same nuclei, but for also acting in the control of the arterial pressure. Both angiotensinergic and glutamatergic systems interact with the catecholaminergic system throughout the nervous system. However, little is known about how the catecholaminergic system interacts with these systems in the modulation of blood pressure. Therefore, we studied in this project the influence of the glutamatergic and angiotensinergic systems over the catecholaminergic system in the medulla oblongata of rats. Through cell cultures of the medulla oblongata, we demonstrated that the activation of glutamatergic NMDA receptors is capable of elevating the proteic levels of α2-adrenoceptors, and that non-NMDA receptors need to be unblocked for such. In adult rats, repeated microinjections inhibit the bradycardic response elicited by the α2 adrenoceptors in the NTS. However, the angiotensin AT1 receptors knockdown restored the bradycardic response. Through the chronic knockout of angiotensinergic AT1 receptors in the NTS, we observed bradycardic response elicited by the activation of α2 adrenoceptors in the NTS of the knock-down rats. These results suggest that the medullary neurotransmission systems interact in different ways, and the comprehension of this control may be of great value for the comprehension of how the neural control of the blood pressure works
 
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Publishing Date
2015-02-20
 
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