Glutamate and its ionotropic receptor agonists inhibit the response to acute hypoxia in carotid body of rats / 生理学报
Acta Physiologica Sinica
;
(6): 537-543, 2023.
Artigo
em Chinês
| WPRIM
| ID: wpr-1007769
ABSTRACT
The purpose of this study was to investigate the effect of glutamate and its ionotropic receptor agonists on the response to acute hypoxia in rat carotid body in vitro. Briefly, after SD rats were anesthetized and decapitated, the bilateral carotid bifurcations were rapidly isolated. Then bifurcation was placed into a recording chamber perfused with 95% O2-5% CO2 saturated Kreb's solution. The carotid body-sinus nerve complex was dissected, and the carotid sinus nerve discharge was recorded using a suction electrode. To detect the response of carotid body to acute hypoxia, the chamber was perfused with 5% O2-5% CO2-90% N2 saturated Kreb's solution for a period of 100 s at an interval of 15 min. To observe the effect of glutamate, ionotropic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor agonist AMPA or N-methyl-D-aspartate (NMDA) receptor agonist NMDA on the response to acute hypoxia in rat carotid body, the chamber was perfused with 5% O2-5% CO2-90% N2 saturated Kreb's solution containing the corresponding reagent. The results showed that glutamate (20 μmol/L), AMPA (5 μmol/L) or NMDA (10 μmol/L) inhibited the acute hypoxia-induced enhancement of carotid sinus nerve activity, and these inhibitory effects were dose-dependent. In summary, the activation of glutamate ionotropic receptors appears to exert an inhibitory effect on the response to acute hypoxia in carotid body of rats.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Dióxido de Carbono
/
Corpo Carotídeo
/
N-Metilaspartato
/
Ratos Sprague-Dawley
/
Receptores de N-Metil-D-Aspartato
/
Receptores de AMPA
/
Ácido alfa-Amino-3-hidroxi-5-metil-4-isoxazol Propiônico
/
Ácido Glutâmico
/
Hipóxia
Limite:
Animais
Idioma:
Chinês
Revista:
Acta Physiologica Sinica
Ano de publicação:
2023
Tipo de documento:
Artigo
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