Nitric oxide modulates the cardiovascular effects elicited by acetylcholine in the NTS of awake rats

Nitric oxide modulates the cardiovascular effects elicited by acetylcholine in the NTS of awake rats

Autor Silva, Liana Gouveia da Autor UNIFESP Google Scholar
Dias, Ana Carolina Rodrigues Autor UNIFESP Google Scholar
Furlan, Elaina Autor UNIFESP Google Scholar
Colombari, Eduardo Autor UNIFESP Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Univ Estadual Paulista
Resumo da Silva LG, Rodrigues Dias AC, Furlan E, Colombari E. Nitric oxide modulates the cardiovascular effects elicited by acetylcholine in the NTS of awake rats. Am J Physiol Regul Integr Comp Physiol 295: R1774-R1781, 2008. First published September 24, 2008; doi:10.1152/ajpregu.00559.2007.-Microinjection of acetylcholine chloride (ACh) in the nucleus of the solitary tract (NTS) of awake rats caused a transient and dose-dependent hypotension and bradycardia. Because it is known that cardiovascular reflexes are affected by nitric oxide (NO) produced in the NTS, we investigated whether these ACh-induced responses depend on NO in the NTS. Responses to ACh (500 pmol in 100 nl) were strongly reduced by ipsilateral microinjection of the NOS inhibitor N-G-nitro-L-arginine methyl ester (L-NAME; 10 nmol in 100 nl) in the NTS: mean arterial pressure (MAP) fell by 50 +/- 5 mmHg before L-NAME to 9 +/- 4 mmHg, 10 min after L-NAME, and HR fell by 100 +/- 26 bpm before L-NAME to 20 +/- 10 bpm, 10 min after L-NAME (both P < 0.05). Microinjection of the selective inhibitor of neuronal nitric oxide synthase (nNOS), 1-(2-trifluoromethylphenyl) imidazole (TRIM; 13.3 nmol in 100 nl), in the NTS also reduced responses to ACh: MAP fell from 42 +/- 3 mmHg before TRIM to 27 +/- 6 mmHg, 10 min after TRIM (P < 0.05). TRIM also tended to reduce ACh-induced bradycardia, but this effect was not statistically significant. ACh-induced hypotension and bradycardia returned to control levels 30-45 min after NOS inhibition. Control injections with D-NAME and saline did not affect resting values or the response to ACh. in conclusion, injection of ACh into the NTS of conscious rats induces hypotension and bradycardia, and these effects may be mediated at least partly by NO produced in NTS neurons.
Palavra-chave cholinergic transmission
nitric oxide synthase inhibition
nucleus of the solitary tract
cardiovascular control
Idioma Inglês
Financiador Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Programa de Apoio aos Nucleos de Excelencia
Data de publicação 2008-12-01
Publicado em American Journal of Physiology-regulatory Integrative and Comparative Physiology. Bethesda: Amer Physiological Soc, v. 295, n. 6, p. R1774-R1781, 2008.
ISSN 0363-6119 (Sherpa/Romeo, fator de impacto)
Publicador Amer Physiological Soc
Extensão R1774-R1781
Fonte http://dx.doi.org/10.1152/ajpregu.00559.2007
Direito de acesso Acesso aberto Open Access
Tipo Artigo
Web of Science WOS:000261559700007
Endereço permanente http://repositorio.unifesp.br/handle/11600/31057

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