Cardiovascular responses to microinjection of L-glutamate into the NTS in AV3V-lesioned rats

Cardiovascular responses to microinjection of L-glutamate into the NTS in AV3V-lesioned rats

Autor Vieira, A. A. Google Scholar
Colombari, E. Google Scholar
De Luca, L. A. Google Scholar
Colombari, DSD Google Scholar
Menani, J. V. Google Scholar
Instituição UNESP
Universidade Federal de São Paulo (UNIFESP)
Resumo The excitatory amino acid L-glutamate injected into the nucleus of the solitary tract (NTS) in unanesthetized rats similar to peripheral chemoreceptor activation increases mean arterial pressure (MAP) and reduces heart rate. in this study, we investigated the effects of acute (I day) and chronic (15 days) electrolytic lesions of the preoptic-periventricular tissue surrounding the anteroventral third ventricle (AV3V region) on the pressor and bradycardic responses induced by injections of L-glutamate into the NTS or peripheral chemoreceptor activation in unanesthetized rats. Male Holtzman rats with sham or electrolytic AV3V lesions and a stainless steel cannula implanted into the NTS were used. Differently from the pressor responses (28 +/- 3 mm Hg) produced by injections into the NTS of sham-lesioned rats, L-glutamate (5 nmol/ 100 nl) injected into the NTS reduced MAP (-26 +/- 8 mm Hg) or produced no effect (2 7 turn Hg) in acute and chronic AV3V-lesioned rats, respectively. the bradycardia to L-glutamate into the NTS and the cardiovascular responses to chemoreflex activation with intravenous potassium cyanide or to baroreflex activation with intravenous phenylephrine or sodium nitroprusside were not modified by AV3V lesions. the results show that the integrity of the AV3V region is essential for the pressor responses to L-glutamate into the NTS but not for the pressor responses to chemoreflex activation, suggesting dissociation between the central mechanisms involved in these responses. (C) 2004 Elsevier B.V. All rights reserved.
Assunto baroreceptor
solitary tract
Idioma Inglês
Data 2004-10-29
Publicado em Brain Research. Amsterdam: Elsevier B.V., v. 1025, n. 1-2, p. 106-112, 2004.
ISSN 0006-8993 (Sherpa/Romeo, fator de impacto)
Editor Elsevier B.V.
Extensão 106-112
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000224682700013

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