Participação dos receptores nicotínicos na neurotransmissão da resposta cárdio-vagal do barorreflexo e do reflexo Bezold-Jarisch no núcleo ambíguo de ratos anestesiados

• Ano de defesa: 2007
• Autor(a) principal: Pedrosa, Diego França
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Federal do Espírito Santo; BR; Mestrado em Ciências Fisiológicas; Centro de Ciências da Saúde; UFES; Programa de Pós-Graduação em Ciências Fisiológicas
• Palavras-chave em Português: Nucleus ambiguus; Nicotinic cholinergic receptor; Baroreflex; BezoldJarisch reflex; α-bungarotoxin; Núcleo ambíguo; Receptor colinérgico nicotínico; Barorreflexo; Reflexo Bezold-Jarisch; α-bungarotoxina; DH-β-E; Receptores nicotínicos; Neurotransmissores; Rato como animal de laboratório; Fisiologia; 612
• Link de acesso: http://repositorio.ufes.br/handle/10/7945

Immunohistochemical studies have demonstrated that the nucleus ambiguus (NA) plays a predominant role in the cardio-vagal control. Using the kynurenic acid blockade, previous studies demonstrated that the excitatory aminoacids receptors of NA neurons have an important role in mediating the negative chronotropic response of baroreflex (BRF) and Bezold Jarisch reflex (BJR) in anesthetized rats. However, there are other aspects that need a better understanding, as the role of nicotinic cholinergic receptors in mediating the participation of the reflex bradicardic response, as well as, the possible influence of these receptors on L-glutamate-induced responses in the NA. The goal of the present study was to evaluate the nicotinic cholinergic receptors participation in modulating the cardiovascular responses induced by BRF and BJR activation and to study a possible interaction between the glutamatergic and nicotinic cholinergic neurotransmission in the NA. Male Wistar rats were used. The animals were anesthetized with urethane, paralyzed with succinylcholine and artificially ventilated. The femoral artery and vein were cannulated for cardiovascular recording and for drug administration, respectively. The sympathetic cardiac activity was blocked with atenolol, a β-adrenoceptor antagonist. Microinjections into the NA were performed at the level of the óbex, following the coordinates based in Paxinos and Watson (1998), ±1.7 mm lateral to the midline and -1.4/-1.7mm ventral to the dorsal surface of the óbex. The drugs used in this study were: L-Glu (5 nmol/50 nL), nicotine (0,5; 1; 5 e 10 mM), αbungarotoxin (1 µM), DH-β-E (100 µM) and control solutions (saline, NaCl 0,9%). The BRF was evoked with a continuous phenylephrine infusion (50 µg/mL/min), and the BJR with an intravenous injection of phenylbiguanide (10 µg/Kg). Our results demonstrated that L-Glu microinjected into the NA produced minimum hypotension and consistent bradycardia. The nicotine microinjections produced significant bradicardic and discrete pressure responses at 1 and 5 mM dosis. At 10 mM dosis, neither bradicardic or pressure responses were no longer observed. The DH-β-E unilateral microinjection at NA did not result in significant alterations in L-Glu induced responses, however, the α-bungarotoxin unilateral microinjection attenuated the LGlu and nicotine-induced bradicardic responses. Regarding the cardiovascular reflexes, the blockade with α-bungarotoxin attenuated significantly the BRF, while only the BJR bradicardic response was attenuated. The present results confirm that the NA plays an important role in modulating cardiovascular responses. They also suggest that the α7 nicotinic cholinergic receptors subunits, at Óbex level, participate of BRF and BJR cardio-vagal reflex responses in anesthetized rats. Regarding the glutamatergic neurotransmission, our results showed that the nicotinic cholinergic receptors intervene at glutamatergic cardiovascular responses. However, additional studies are needed to elucidate this interaction occurs at L-glutamate releasing from NTS projections or directly at the excitatory aminoacid receptors in the NA